Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system

Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system Acute care handbook for physical therapists (fourth edition) chapter 6 nervous system

CHAPTER Nervous System Hillary A Reinhold Michele P West CHAPTER OUTLINE CHAPTER OBJECTIVES Body Structure and Function of the Nervous System Central Nervous System Peripheral Nervous System Autonomic Nervous System Neurologic Examination Patient History Observation Mental Status Examination Vital Signs Cranial Nerves Vision Motor Function Diagnostic Procedures X-ray Computed Tomography and Angiography Magnetic Resonance Imaging and Angiography Doppler Flowmetry Digital-Subtraction Angiography Cerebral Angiography Lumbar Puncture Positron Emission Tomography Electroencephalography Evoked Potentials Electromyography and Nerve Conduction Velocity Studies Myelography Transesophageal Echocardiography Health Conditions Traumatic Brain Injury Spinal Cord Injury Cerebrovascular Disease and Disorders Dementia Ventricular Dysfunction Seizure Syncope Neuroinfectious Diseases Vestibular Dysfunction Common Degenerative Central Nervous System Diseases General Management Intracranial and Cerebral Perfusion Pressure Pharmacologic Therapy Neurosurgical Procedures Physical Therapy Intervention The objectives of this chapter are to provide the following: Provide a brief review of the structure and function of the nervous system Give an overview of neurologic evaluation, including the physical examination and diagnostic tests Describe common neurologic diseases and disorders, including clinical findings, medical and surgical management, and physical therapy interventions PREFERRED PRACTICE PATTERNS The most relevant practice patterns for the diagnoses discussed in this chapter, based on the American Physical Therapy Association’s Guide to Physical Therapist Practice, second edition, are as follows: • Common Degenerative Central Nervous System Diseases (Amyotrophic Lateral Sclerosis, Guillain-Barré Syndrome, Multiple Sclerosis, Parkinson’s Disease, Huntington’s Disease): 5A, 5E, 5G, 6B, 6E, 7A • Vestibular Dysfunction (Bilateral Vestibular Hypofunction, Ménière’s Disease, Acute Vestibular Neuronitis, Benign Positional Paroxysmal Vertigo, Vertigo, Lightheadedness, Dysequilibrium): 5A • Neuroinfectious diseases (Encephalitis, Meningitis, and Poliomyelitis [more information in Chapter 13]): 4A, 5C, 5D, 5G, 5H, 6E, 7A • Syncope: 5A • Seizure (Status Epilepticus, Epilepsy, Simple Partial Seizures, Complex Partial Seizures, Tonic-Clonic Seizures): 5A, 5C, 5D, 5E • Ventricular Dysfunction (Cerebrospinal Fluid Leak and Hydrocephalus): 5C, 5D • Spinal Cord Injury: 5H, 7A, 7C • Traumatic Brain Injury: 5C, 5D, 5I • Cerebrovascular Disease and Disorders (Transient Ischemic Attack, Cerebrovascular Accident, Dementia, Subarachnoid Hemorrhage, Arteriovenous Malformation and Cerebral Aneurysm): 5C, 5D, 5I, 6E, 6F, 7A Please refer to Appendix A for a complete list of the preferred practice patterns, as individual patient conditions are highly variable and other practice patterns may be applicable The nervous system is linked to every system of the body and is responsible for the integration and regulation of homeostasis It is also involved in the action, communication, and higher cortical function of the body A neurologic insult and its manifestations therefore have the potential to affect multiple body systems To safely and effectively prevent or improve the neuromuscular, systemic, and functional sequelae of altered neurologic status in the acute care setting, the physical therapist requires an understanding of the neurologic system and the principles of neuropathology Body Structure and Function of the Nervous System The nervous system is divided as follows: • The central nervous system (CNS), consisting of the brain and spinal cord • The peripheral nervous system, consisting of efferent and afferent nerves outside the CNS 123 124 CHAPTER 6    Nervous System The peripheral nervous system is divided into: • The autonomic (involuntary) nervous system, consisting of the sympathetic and parasympathetic systems innervating the viscera, smooth muscles, and glands • The somatic (voluntary) nervous system, consisting of efferent and afferent nerves to all parts of the body except the viscera, smooth muscles, and glands Central Nervous System Brain The brain is anatomically divided into the cerebral hemispheres, diencephalon, brain stem, and cerebellum A midsagittal view of the brain is shown in Figure 6-1, A Figure 6-1, B shows the basal ganglia and the internal capsule Although each portion of the brain has its own function, it is linked to other portions via tracts and rarely works in isolation When lesions occur, disruption of these functions can be predicted Tables 6-1 and 6-2 describe the basic structure, function, and dysfunction Corpus callosum of the cerebral hemispheres, diencephalon, brain stem, and cerebellum Protective Mechanisms.  The brain is protected by the cranium, meninges, ventricular system, and blood-brain barrier Cranium.  The cranium encloses the brain It is composed of eight cranial and 14 facial bones connected by sutures and contains approximately 85 foramina for the passage of the spinal cord, cranial nerves (CNs), and blood vessels.1 The cranium is divided into the cranial vault, or calvaria (the superolateral and posterior aspects), and the cranial floor, which is composed of fossae (the anterior fossa supports the frontal lobes; the middle fossa supports the temporal lobes; and the posterior fossa supports the cerebellum, pons, and medulla).2 Meninges.  The meninges are three layers of connective tissue that cover the brain and spinal cord The dura mater, the outermost layer, lines the skull (periosteum) and has four major folds (Table 6-3) The arachnoid, the middle layer, loosely encloses the brain The pia mater, the inner layer, covers the convolutions of the brain and forms a portion of the choroid plexus in the ventricular system The three layers create very PARIETAL LOBE Cingulate gyrus FRONTAL LOBE LIMBIC LOBE OCCIPITAL LOBE Hippocampus Thalamus DIENCEPHALON Amygdala Hypothalamus Pituitary gland Midbrain BRAIN STEM A Pons CEREBELLUM SPINAL CORD Medulla B FIGURE 6-1  A, Schematic midsagittal view of the brain shows the relationship between the cerebral cortex, cerebellum, spinal cord, and brainstem and the subcortical structures important to functional movement B, Horizontal section of the cerebrum showing the basal ganglia (A, From Cech DJ, Martin ST: Functional movement development across the life span, ed 3, St Louis, 2012, Saunders B, From Love RJ, Webb WG, editors: Neurology for the speech-language pathologist, ed 4, Boston, 2001, Butterworth-Heinemann, p 38.) CHAPTER 6    Nervous System 125 TABLE 6-1  Structure, Function, and Dysfunction of the Cerebral Hemispheres Lobe of Cerebrum Structure Function Dysfunction Frontal lobe Precentral gyrus Voluntary motor cortex of contralateral face, arm, trunk, and leg Advanced motor planning Contralateral head and eye turning (connections to cranial nerves III, IV, VI, IX, X, and XII nuclei) Personality center, including abstract ideas, concern for others, conscience, initiative, judgment, persistence, and planning Contralateral mono- or hemiparesis or hemiplegia Contralateral head and eye paralysis Akinesia or inability to perform complex tasks Supplementary motor area Prefrontal pole Paracentral lobule Broca’s area Parietal lobe Postcentral gyrus Parietal pole Wernicke’s area Temporal lobe Optic radiation Gustatory cortex Superior temporal gyrus (auditory cortex) Middle and inferior temporal gyri Limbic lobe and olfactory cortex Wernicke’s area Optic radiation Occipital lobe Striate and parastriate cortices Bladder and bowel inhibition D: Motor speech center ND: Appreciation of intonation and gestures with vocalization Somatosensory cortex of contralateral pain; posture; proprioception; touch of arm, trunk, and leg D: Ability to perform calculations ND: Ability to construct shapes, awareness of external environment, and body image D: Sensory speech (auditory and written) comprehension center ND: Appreciation of content of emotional language (e.g., tone of voice) Visual tract Perception of taste D: Appreciation of language ND: Appreciation of music, rhythm, and sound Learning and memory centers Affective and emotion center, including mood, primitive behavior, selfpreservation, short-term memory, visceral emotion processes, and interpretation of smell See Parietal lobe, above Visual tract Perception of vision (visual cortex) Loss of inhibition and demonstration of antisocial behaviors Ataxia, primitive reflexes, and hypertonicity Urinary and bowel incontinence Broca’s (expressive) aphasia Contralateral sensation loss D: Acalculia, agraphia, finger agnosia ND: Constructional apraxia, geographic agnosia, dressing apraxia, anosognosia Wernicke’s (receptive) aphasia Lower homonymous quadrantanopia Dysfunction is very uncommon D: Decreased ability to hear ND: Decreased ability to appreciate music Learning and memory deficits Aggressive or antisocial behaviors Inability to establish new memories Wernicke’s (receptive) aphasia Upper homonymous quadrantanopia Homonymous hemianopsia with or without macular involvement Data from Gilman S, Newman SW, editors: Manter and Gatz’s essentials of clinical neuroanatomy and neurophysiology, ed 7, Philadelphia, 1989, FA Davis; Kiernan JA, editor: Introduction to human neuroscience, Philadelphia, 1987, Lippincott; Marieb EN, editor: Human anatomy and physiology, ed 5, San Francisco, 2001, Benjamin-Cummings; Thelan L, Davie J, Lough M, editors: Critical care nursing: diagnosis and management, ed 2, St Louis, 1994, Mosby; Mancell EL, editor: Gray’s clinical neuroanatomy: the anatomic basis for clinical neuroscience, Philadelphia, 2011, Elsevier Saunders; O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation, ed 5, Philadelphia, 2007, FA Davis D, Dominant; ND, nondominant important anatomic and potential spaces in the brain, as shown in Figure 6-2 and described in Table 6-4 Ventricular System.  The ventricular system nourishes the brain and acts as a cushion by increasing the buoyancy of the brain It consists of four ventricles and a series of foramina, through which cerebrospinal fluid (CSF) passes to surround the CNS CSF is a colorless, odorless solution produced by the choroid plexus of all ventricles at a rate of 400 to 500 ml per day.2 CSF circulates in a pulse-like fashion through the ventricles and around the spinal cord with the beating of ependymal cilia that line the ventricles and intracranial blood volume changes that occur with breathing and cardiac systole.3 The flow of CSF under normal conditions, as shown in Figure 6-3, is as follows4: • From the lateral ventricles via the interventricular foramen to the third ventricle • From the third ventricle to the fourth ventricle via the cerebral aqueduct 126 CHAPTER 6    Nervous System TABLE 6-2  Structure, Function, and Dysfunction of the Diencephalon, Brain Stem, and Cerebellum Brain Structure Substructure Function Dysfunction Diencephalon Thalamus Specific and association nuclei Cortical arousal Integrative relay station for all ascending and descending motor stimuli and all ascending sensory stimuli except smell Memory Autonomic center for sympathetic and parasympathetic responses Visceral center for regulation of body temperature, food intake, thirst, sleep and wake cycle, water balance Produces ADH and oxytocin Regulates anterior pituitary gland Association with limbic system Association with limbic system Altered consciousness Signs and symptoms of increased ICP Contralateral hemiplegia, hemiparesis, or hemianesthesia Altered eye movement Thalamic pain syndrome Altered autonomic function and vital signs Headache Visual deficits Vomiting with signs and symptoms of increased ICP See Chapter 10 for more information on hormones and endocrine disorders Dysfunction unknown Association with thalamus for motor control Production, storage, and secretion of reproductive hormones Secretion of ADH and oxytocin Conduction pathway between the cortex and spinal cord Dyskinesia and decreased motor control See Chapter 10 for more information on hormones and endocrine disorders Contralateral hemiparesis or hemiplegia and hemianesthesia Superior cerebellar peduncles Superior and inferior colliculi Medial and lateral lemniscus CNs III and IV nuclei Reticular formation Cerebral aqueduct in its center Middle cerebellar peduncles Respiratory center CNs V-VIII nuclei Forms anterior wall of fourth ventricle Decussation of pyramidal tracts Inferior cerebellar peduncles Inferior olivary nuclei Nucleus cuneatus and gracilis CNs IX-XII nuclei Conduction pathway between higher and lower brain centers Visual reflex Auditory reflex Contralateral hemiparesis or hemiplegia and hemianesthesia, altered consciousness and respiratory pattern, cranial nerve palsy Conduction pathway between higher and lower brain centers See Midbrain, above Homeostatic center for cardiac, respiratory, vasomotor functions See Midbrain, above Medial portion Lateral portion Sensory and motor input of trunk Sensory and motor input of extremities for coordination of gait Sensory and motor input for coordination of motor skills and postural tone Sensory input from ears Sensory and motor input from eyes and head for coordination of balance and eye and head movement Ipsilateral ataxia and discoordination or tremor of extremities Hypothalamus Mamillary bodies Optic chiasm Infundibulum (stalk) connects to the pituitary gland Forms inferolateral wall of third ventricle Epithalamus Pineal body Posterior commissure, striae medullares, habenular nuclei and commissure Substantia nigra Red nuclei Anterior and posterior lobes Subthalamus Pituitary Internal capsule Brain Stem Midbrain Pons Medulla Cerebellum Anterior lobe Fiber tracts connecting thalamus to the cortex Posterior lobe Medial and lateral portions Flocculonodular Flocculus nodule Ipsilateral ataxia and discoordination of the trunk Ipsilateral facial sensory loss and Horner’s syndrome, nystagmus, visual overshooting Loss of balance Data from Gilman S, Newman SW, editors: Manter and Gatz’s essentials of clinical neuroanatomy and neurophysiology, ed 7, Philadelphia, 1989, FA Davis; Kiernan JA, editor: Introduction to human neuroscience, Philadelphia, 1987, Lippincott; Marieb EN, editor: Human anatomy and physiology, ed 5, San Francisco, 2001, Benjamin-Cummings; Thelan L, Davie J, Lough M, editors: Critical care nursing: diagnosis and management, ed 2, St Louis, 1994, Mosby; Mancell EL, editor: Gray’s clinical neuroanatomy: the anatomic basis for clinical neuroscience, Philadelphia, 2011, Elsevier Saunders; O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation, ed 5, Philadelphia, 2007, FA Davis ADH, Antidiuretic hormone; CN, cranial nerve; ICP, intracranial pressure CHAPTER 6    Nervous System TABLE 6-3  Dural Folds TABLE 6-4  Dural Spaces Falx cerebri Epidural (extradural) space Subdural space Falx cerebelli Tentorium cerebelli Diaphragm sellae Vertical fold that separates the two cerebral hemispheres to prevent horizontal displacement of these structures Vertical fold that separates the two cerebellar hemispheres to prevent horizontal displacement of these structures Horizontal fold that separates occipital lobes from the cerebellum to prevent vertical displacement of these structures Horizontal fold that separates the subarachnoid space from the sella turcica and is perforated by the stalk of the pituitary gland Subarachnoid space 127 Potential space between the skull and outer dura mater Potential space between the dura and the arachnoid mater; a split in the dura contains the venous sinus Anatomic space between the arachnoid and pia mater containing cerebrospinal fluid and the vascular supply of the cortex Data from Wilkinson JL, editor: Neuroanatomy for medical students, ed 3, Oxford, UK, 1998, Butterworth-Heinemann FIGURE 6-2  Coronal section of cranial meninges showing a venous sinus and dural fold (From Young PA, Young PH: Basic clinical neuroanatomy, Philadelphia, 1997, Williams & Wilkins, p 8.) FIGURE 6-3  The ventricular system of the brain Arrows indicate the circulation of cerebrospinal fluid from the site of formation in the choroid plexus to the site of absorption in the villi of the sagittal sinus (From Bogousslavsky J, Fisher M, editors: Textbook of neurology, Boston, 1998, Butterworth-Heinemann, p 656.) 128 CHAPTER 6    Nervous System TABLE 6-5  Blood Supply of the Major Areas of the Brain Artery Anterior Circulation Internal carotid artery (ICA) External carotid artery (ECA) Anterior cerebral artery (ACA) FIGURE 6-4  Schematic representation of the arterial circle of Willis and accompanying veins Ant., Anterior; art., artery; Post., posterior (From Gonzalez EG, Meyers SJ, editors: Downey and Darling’s physiological basis of rehabilitation medicine, ed 3, Boston, 2001, Butterworth-Heinemann, p 22.) • From the fourth ventricle to the cisterns, subarachnoid space, and spinal cord via the median and lateral apertures When ventricular pressure is greater than venous pressure, CSF is absorbed into the venous system via the arachnoid villi, capillary walls of the pia mater, and lymphatics of the subarachnoid space near the optic nerve.2 Blood-Brain Barrier.  The blood-brain barrier is the physiologic mechanism responsible for keeping toxins, such as amino acids, hormones, ions, and urea, from altering neuronal firing of the brain It readily allows water, oxygen, carbon dioxide, glucose, some amino acids, and substances that are highly soluble in fat (e.g., alcohol, nicotine, and anesthetic agents) to pass across the barrier.5,6 The barrier consists of fused endothelial cells on a basement membrane that is surrounded by astrocytic foot extensions.6 Substances must therefore pass through, rather than around, these cells The blood-brain barrier is absent near the hypothalamus, pineal region, anterior third ventricle, and floor of the fourth ventricle.3 Central Brain Systems.  The central brain systems are the reticular activating system and the limbic system The reticular activating system (RAS) is composed of an ascending tract and a descending tract The ascending RAS is responsible for human consciousness level and integrates the functions of the brain stem with cortical, cerebellar, thalamic, hypothalamic, and sensory receptor functions.5 The descending RAS promotes spinal cord antigravity reflexes or extensor tone needed to maintain standing.7 The limbic system is a complex interactive system, with primary connections between the cortex, hypothalamus, amygdala, and sensory receptors The limbic system plays a major role in memory, emotion, and visceral and motor responses involved in defense and reproduction by mediating cortical autonomic function of internal and external stimuli.8,9 Circulation.  The brain receives blood from the internal carotid and vertebral arteries, which are linked together by the circle of Willis, as shown in Figure 6-4 Each vessel supplies blood to a certain part of the brain (Table 6-5) The circulation of the brain is discussed in terms of a single vessel or by region Middle cerebral artery (MCA) Posterior Circulation Vertebral artery Basilar artery Posterior inferior cerebellar artery (PICA) Anterior inferior cerebellar artery (AICA) Superior cerebellar artery (SCA) Posterior cerebral artery (PCA) Area of Perfusion The dura, optic tract, basal ganglia, midbrain, uncus, lateral geniculate body, pituitary gland, trigeminal ganglion, and tympanic cavity Ophthalmic branch supplies the eyes and orbits All structures external to the skull, the larynx, and the thyroid Medial and superior surface of frontal and parietal lobes Medial striate branch supplies anterior portion of the internal capsule, optic chiasm and nerve, portions of the hypothalamus, and basal ganglia Lateral surface of the frontal, parietal, and occipital lobes, including the superior and lateral surfaces of temporal lobes, posterior portion of the internal capsule, and portions of the basal ganglia Medulla, dura of the posterior fossa, including the falx cerebri and tentorium cerebelli Pons, midbrain, internal ear, cerebellum Posterior and inferior surface of the cerebellum, choroid plexus of the fourth ventricle Anterior surface of the cerebellum, flocculus, and inferior vermis Superior surface of the cerebellum and vermis Occipital lobe and medial and lateral surfaces of the temporal lobes, thalamus, lateral geniculate bodies, hippocampus, and choroid plexus of the third and lateral ventricles Data from Rumbaugh CL, Wang A, Tsai FY, editors: Cerebrovascular disease imaging and interventional treatment options, New York, 1995, Igaku-Shoin Medical Publishers; Moore KI, Dalley AF, editors: Clinically oriented anatomy, ed 4, Baltimore, 1999, Lippincott Williams & Wilkins; O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation, ed 5, Philadelphia, 2007, FA Davis (usually as the anterior or posterior circulation) There are several anastomotic systems of the cerebral vasculature that provide essential blood flow to the brain Blood is drained from the brain through a series of venous sinuses The superior sagittal sinus, with its associated lacunae and villi, is the primary drainage site The superior sagittal sinus and sinuses located in the dura and scalp then drain blood into the internal jugular vein for return to the heart Spinal Cord The spinal cord lies within the spinal column and extends from the foramen magnum to the first lumbar vertebra, where it CHAPTER 6    Nervous System 129 FIGURE 6-5  Cross-section of the spinal cord Ant., Anterior; Lat., lateral; Post., posterior (From Love RJ, Webb WG, editors: Neurology for the speech-language pathologist, ed 4, Boston, 2001, Butterworth-Heinemann, p 44.) forms the conus medullaris and the cauda equina and attaches to the coccyx via the filum terminale Divided into the cervical, thoracic, and lumbar portions, it is protected by mechanisms similar to those supporting the brain The spinal cord is composed of gray and white matter and provides the pathway for the ascending and descending tracts, as shown in cross-section in Figure 6-5 and outlined in Table 6-6 TABLE 6-6  Major Ascending and Descending White Matter Tracts* Tract Function Fasciculus gracilis Sensory pathway for lower-extremity and lower-trunk joint proprioception, vibration, two-point discrimination, graphesthesia, and double simultaneous stimulation Sensory pathway for upper-extremity, upper-trunk, and neck joint proprioception, vibration, two-point discrimination, graphesthesia, and double simultaneous stimulation Sensory pathway for pain, temperature, and light touch Sensory pathway for ipsilateral subconscious proprioception Sensory pathway for ipsilateral and contralateral subconscious proprioception Motor pathway for contralateral voluntary fine-muscle movement Motor pathway for ipsilateral voluntary movement Motor pathway for gross postural tone Peripheral Nervous System The peripheral nervous system consists of the cranial and spinal nerves and the reflex system The primary structures include peripheral nerves, associated ganglia, and sensory receptors There are 12 pairs of CNs, each with a unique pathway and function (sensory, motor, mixed, or autonomic) Thirty-one pairs of spinal nerves (all mixed) exit the spinal cord to form distinct plexuses (except T2 to T12) The peripheral nerves of the trunk and the upper and lower extremities are listed in Table 6-7, and the dermatomal system is shown in Figure 6-6 The reflex system includes spinal, deep tendon, stretch, and superficial reflexes and protective responses Autonomic Nervous System The portion of the peripheral nervous system that innervates glands and cardiac and smooth muscle is the autonomic nervous system The parasympathetic division is activated in times of rest, whereas the sympathetic division is activated in times of work or “fight or flight” situations The two divisions work closely together, with dual innervation of most organs, to ensure homeostasis Neurologic Examination The neurologic examination is initiated on hospital admission or in the field and is reassessed continuously, hourly, or daily, as necessary The neurologic examination consists of patient Fasciculus cuneatus Lateral spinothalamic Ventral spinocerebellar Dorsal spinocerebellar Lateral corticospinal (pyramidal) Anterior corticospinal (pyramidal) Rubrospinal (extrapyramidal) Tectospinal (extrapyramidal) Vestibulospinal (extrapyramidal) Motor pathway for contralateral gross postural muscle tone associated with auditory and visual stimuli Motor pathway for ipsilateral gross postural adjustments associated with head movements Data from Gilman S, Newman SW, editors: Manter and Gatz’s essentials of clinical neuroanatomy and neurophysiology, ed 7, Philadelphia, 1989, FA Davis; Marieb EN, editor: Human anatomy and physiology, ed 5, San Francisco, 2001, Benjamin-Cummings *Sensory tracts ascend from the spinal cord; motor tracts descend from the brain to the spinal cord 130 CHAPTER 6    Nervous System TABLE 6-7  Major Peripheral Nerves of the Trunk, Upper Extremity, and Lower Extremity Nerve Spinal Root Innervation Iliohypogastric and ilioinguinal C3 and C4 C3, C4, and C5 C5, C6, and C7 C6, C7, and C8 C7, C8, and T1 C7 and C8 Corresponds to nerve root level L1 Trapezius Diaphragm Serratus anterior Pectoralis minor and major Pectoralis major Latissimus dorsi External intercostals, internal intercostals, levatores costarum longi and brevis Transversus abdominis, internal abdominal oblique Upper Extremity Dorsal scapular Suprascapular Lower subscapular Upper subscapular Axillary Radial C5 C5 and C6 C5 and C6 C5 and C6 C5 and C6 C5, C6, C7, C8, and T1 Ulnar C8 and T1 Median C6, C7, C8, and T1 Musculocutaneous C5, C6, and C7 Levator scapulae, rhomboid major and minor Supraspinatus, infraspinatus, and glenohumeral joint Teres major and inferior portion of subscapularis Superior portion of subscapularis Teres minor, deltoid, and glenohumeral joint Triceps, brachioradialis, anconeus, extensor carpi radialis longus and brevis, supinator, extensor carpi ulnaris, extensor digitorum, extensor digiti minimi, extensor indicis, extensor pollicis longus and brevis, abductor pollicis brevis Flexor digitorum profundus, flexor carpi ulnaris, palmaris brevis, abductor digiti minimi, flexor digiti minimi brevis, opponens digiti minimi, palmar and dorsal interossei, third and fourth lumbricals Pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis and profundus, flexor pollicis longus, pronator quadratus, abductor pollicis brevis, opponens pollicis, flexor pollicis brevis, first and second lumbricals Coracobrachialis, brachialis, biceps Lower Extremity Femoral L2, L3, and L4 Obturator L2, L3, and L4 Superior gluteal Inferior gluteal Sciatic Tibial L4, L5, and S1 L5, S1, and S2 L4, L5, S1, S2, and S3 L4, L5, S1, S2, and S3 Common peroneal L4, L5, S1, and S2 Trunk Spinal accessory Phrenic Long thoracic Medial pectoral Lateral pectoral Thoracodorsal Intercostal Iliacus, psoas major, sartorius, pectinous, rectus femoris, vastus lateralis, intermedius, and medialis, articularis genu Obturator externus, adductor brevis, longus, and magnus, gracilis, pectineus Gluteus medius and minimus, tensor fasciae latae Gluteus maximus Biceps femoris, adductor magnus, semitendinosus, semimembranosus Gastrocnemius, soleus, flexor digitorum longus, tibialis posterior, flexor hallucis longus Peroneus longus and brevis, tibialis anterior, extensor digitorum longus, extensor hallucis longus, extensor hallucis brevis, extensor digitorum brevis Data from Netter FH, editor: Atlas of human anatomy, Summit City, NJ, 1989, Ciba-Geigy; Moore KL, Dalley AF, editors: Clinically oriented anatomy, ed 4, Baltimore, 1999, Lippincott Williams & Wilkins history; observation; mental status examination; vital sign measurement; vision, motor, sensory, and coordination testing; and diagnostic testing Patient History A detailed history, initially taken by the physician, is often the most helpful information used to delineate whether a patient presents with a true neurologic event or another process (usually cardiac or metabolic in nature) The history may be presented by the patient or, more commonly, by a family member or person witnessing the acute or progressive event(s) responsible for hospital admission One common framework for organizing questions regarding each neurologic complaint, sign, or symptom is as follows10,11: • What is the patient feeling? • When did the problem initially occur, and has it progressed? • What relieves or exacerbates the problem? • What are the onset, frequency, and duration of signs or symptoms? In addition to the general medical record review (see Chapter 2), questions relevant to a complete neurologic history include: • Does the problem involve loss of consciousness? • Did a fall precede or follow the problem? • Is there headache, dizziness, or visual disturbance? • What are the functional deficits associated with the problem? • Is there an alteration of speech? CHAPTER 6    Nervous System 131 FIGURE 6-6  Dermatome chart based on embryologic segments (From Maitland GD, editor: Vertebral manipulation, ed 5, Oxford, UK, 1986, Butterworth-Heinemann, p 46.) • Does the patient demonstrate memory loss or altered cognition? • Does the patient have an altered sleep pattern? • What is the handedness of the patient? (Handedness is a predictor of brain [language] dominance.) Observation Data that can be gathered from close or distant observation of the patient include the following: • Level of alertness, arousal, distress, or the need for restraint • Body position • Head, trunk, and extremity posture, including movement patterns • Amount and quality of active movement • Amount and quality of interaction with the environment or family members • Degree of ease or difficulty with activities of daily living • Presence of involuntary movements, such as tremor • Eye movement(s) • Presence of hemibody or hemispace neglect • Presence of muscle atrophy • Respiratory rate and pattern • Facial expression and symmetry The therapist should correlate these observations with other information from the chart review and other health care team members to determine: If the diagnosis is consistent with the physical presentation, What types of commands or tone of voice to use, How much assistance is needed, and How to prioritize the portions of the physical therapy evaluation Mental Status Examination The mental status examination includes assessment of level of consciousness, cognition, emotional state, memory, and speech and language ability Level of Consciousness Consciousness consists of arousal and the awareness of self and environment, including the ability to interact appropriately in response to any normal stimulus.12 Coma is often considered the opposite of consciousness Table 6-8 describes the different states of consciousness Evaluating a patient’s level of consciousness is important because it serves as a baseline to monitor stability, improvement, or decline in the patient’s condition It also helps to determine the severity and prognosis of neurologic insult or disease state, thus directing the medical plan of care Physical Therapy Implications.  Time of day, fatigue, and side effects of medication are factors that can cause variable levels of alertness or participation in physical therapy The documentation of these factors is important for communication 132 CHAPTER 6    Nervous System TABLE 6-8  Normal and Abnormal States of Consciousness TABLE 6-9  Glasgow Coma Scale Alert Eye opening (E) Lethargic or somnolent Obtunded Stupor (semicoma) Coma (deep coma) Delirium Dementia Completely awake Attentive to normal levels of stimulation Able to interact meaningfully with clinician Arousal with stimuli Falls asleep when not stimulated Decreased awareness Loss of train of thought Difficult to arouse Requires constant stimulation to maintain consciousness Confused when awake Interactions with clinicians may be largely unproductive Arousal only with strong, generally noxious stimuli and returns to unconscious state when stimulation is stopped Patient is unable to interact with clinician Unarousable to any type of stimulus Reflex motor responses may or may not be seen State of disorientation marked by irritability or agitation, paranoia, and hallucinations Patient demonstrates offensive, loud, and talkative behaviors Alteration in mental processes secondary to organic disease that is not accompanied by a change in arousal among the health care team and for the rehabilitation screening process A progressive intensity of stimuli should be used to arouse a patient with decreased alertness or level of consciousness For example, call the patient’s name in a normal tone of voice before using a loud tone of voice, or tap the patient’s shoulder before rubbing the shoulder Changes in body position, especially the transition from a recumbent position to sitting upright, can also be used to stimulate increased alertness Other stimuli to increase alertness include daylight, radio or television sound, or a cold cloth on the forehead Glasgow Coma Scale.  The Glasgow Coma Scale (GCS) is a widely accepted measure of level of consciousness and responsiveness and is described in Table 6-9 The GCS evaluates best eye opening (E), motor response (M), and verbal response (V) To determine a patient’s overall GCS, add each score (i.e., E + M + V) Scores range from to 15 A score of or less signifies coma.13 Calculation of the GCS usually occurs at regular intervals The GCS should be used to confirm the type and amount of cueing needed to communicate with a patient, determine what time of day a patient is most capable of participating in physical therapy, and delineate physical therapy goals Cognition Cognitive testing includes the assessment of attention, orientation, memory, abstract thought, and the ability to perform Response Motor response (M) Verbal response (V) Score Spontaneous: eyes open without stimulation To speech: eyes open to voice To pain: eyes open to noxious stimulus Nil: eyes not open despite variety of stimuli Obeys: follows commands Localizes: purposeful attempts to move limb to stimulus Withdraws: flexor withdrawal without localizing Abnormal flexion: decorticate posturing to stimulus Extensor response: decerebrate posturing to stimulus Nil: no motor movement Oriented: normal conversation Confused conversation: vocalizes in sentences, incorrect context Inappropriate words: vocalizes with comprehensible words Incomprehensible words: vocalizes with sounds Nil: no vocalization 5 Data from Teasdale G, Jennett B: Assessment of coma and impaired consciousness: a practical scale, Lancet 2:81, 1974 calculations or construct figures General intelligence and vocabulary are estimated with questions regarding history, geography, or current events Table 6-10 lists typical methods of testing the components of cognition   CLINICAL TIP A & O × is a common abbreviation for alert and oriented to person, place, and time The number may be modified to reflect the patient’s orientation (e.g., A & O × [self]) A & O × may also be used to identify that the patient is oriented to the situation Emotional State Emotional state assessment entails observation and direct questioning to ascertain a patient’s mood, affect, perception, and thought process, as well as to evaluate for behavioral changes Evaluation of emotion is not meant to be a full psychiatric examination; however, it provides insight as to how a patient may complete the cognitive portion of the mental status examination.14 It is important to note that a patient’s culture may affect particular emotional responses Patients who recently have had a stroke or have a history of stroke, for example, can be emotionally labile depending on the site of the lesion This can be quite 146 CHAPTER 6    Nervous System TABLE 6-22  Neurologic Signs Associated with CVA by Location Artery Affected Neurologic Signs Internal carotid artery supplies the diencephalon and the cerebral hemispheres via the middle cerebral artery and the anterior cerebral artery Middle cerebral artery supplies the frontal lobe, parietal lobe, and cortical surfaces of temporal lobe (affecting structures of higher cerebral processes of communication; language interpretation; and perception and interpretation of space, sensation, form, and voluntary movement) Anterior cerebral artery supplies superior surfaces of frontal and parietal lobes and medial surface of cerebral hemispheres (includes motor and somesthetic cortex serving the legs), basal ganglia, and corpus callosum Unilateral blindness Severe contralateral hemiplegia and hemianesthesia Profound aphasia Alterations in communication, cognition, mobility, and sensation Contralateral homonymous hemianopsia Contralateral hemiplegia or hemiparesis, motor and sensory loss, greater in the face and arm than in the leg Posterior cerebral artery supplies medial and inferior temporal lobes, medial occipital lobe, thalamus, posterior hypothalamus, and visual receptive area Vertebral or basilar arteries supply the brain stem and cerebellum   Incomplete occlusion   Anterior portion of the pons   Complete occlusion or hemorrhage Posterior inferior cerebellar artery supplies the lateral and posterior portion of the medulla Anterior inferior and superior cerebellar arteries supply the cerebellum Emotional lability Confusion, amnesia, personality changes Urinary incontinence Contralateral hemiplegia or hemiparesis, greater in the leg than in the arm Hemianesthesia Contralateral hemiplegia, greater in the face and arm than in the leg Cerebellar ataxia, tremor Homonymous hemianopsia, cortical blindness Receptive aphasia Memory deficits Weber’s syndrome Unilateral and bilateral weakness of extremities; upper motor neuron weakness involving face, tongue, and throat; loss of vibratory sense, two-point discrimination, and position sense Diplopia, homonymous hemianopsia Nausea, vertigo, tinnitus, and syncope Dysphagia, dysarthria Sometimes confusion and drowsiness “Locked-in” syndrome—no movement except eyelids; sensation and consciousness preserved Coma or death Miotic pupils Decerebrate rigidity Respiratory and circulatory abnormalities Wallenberg syndrome Dysphagia, dysphonia Nystagmus, vertigo, nausea, and vomiting Ipsilateral anesthesia of face and cornea for pain and temperature (touch preserved) Contralateral anesthesia of trunk and extremities for pain and temperature Ipsilateral Horner syndrome Ipsilateral decompensation of movement Difficulty with articulation, gross movements of limbs—ipsilateral ataxia Nystagmus, vertigo, nausea, and vomiting Ipsilateral Horner syndrome Data from Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms, J Neurosurg 28(1):14-20, 1968; Hunt WE, Meagher JN, Hess RM: Intracranial aneurysm: a nine-year study, Ohio State Med J 62(11):1168-1171, 1966 • Watershed stroke: A cerebral infarct between the terminal areas of perfusion of two different arteries, typically between the anterior and middle cerebral arteries17 Arteriovenous Malformation AVM is a malformation in which blood from the arterial system is shunted to the venous system (thereby bypassing the capillaries) through abnormally thin and dilated vessels, making them prone to ruptures causing intracerebral hemorrhage An AVM can occur in a variety of locations, shapes, and sizes The result of the bypass of blood is degeneration of brain parenchyma around the site of the AVM, which creates a chronic ischemic state Signs and symptoms of AVM include headache, dizziness, fainting, seizure, aphasia, bruit, and motor and sensory deficits.64 Management of AVM includes cerebral angiogram to evaluate the precise location of the AVM, followed by CHAPTER 6    Nervous System TABLE 6-23  Focal Signs in Patients with Aneurysms at Various Sites TABLE 6-24  Hunt and Hess Scale for Measuring Subarachnoid Hemorrhage Site of Aneurysms Clinical Findings I Internal carotid—post communicating Middle cerebral artery Cranial nerve III palsy Anterior communicating Basilar artery apex Intracranial vertebral artery/posterior inferior cerebellar artery Contralateral face or hand paresis Aphasia (left side) Contralateral visual neglect (right side) Bilateral leg paresis Bilateral Babinski sign Vertical gaze paresis Coma Vertigo Elements of lateral medullary syndrome From Goetz CG, editor: Textbook of clinical neurology, ed 2, Philadelphia, 2003, Saunders surgical AVM repair, embolization, radiosurgery (stereotactic), photon beam therapy, or medical management alone with close monitoring in some cases.43 Cerebral Aneurysm Cerebral aneurysm is the dilation of a cerebral blood vessel wall owing to a smooth muscle defect through which the endothelial layer penetrates Cerebral aneurysms most commonly occur at arterial bifurcations and in the larger vessels of the anterior circulation Signs and symptoms of unruptured cerebral aneurysm are determined by size and location, detailed in Table 6-23 When an aneurysm ruptures, blood is released under arterial pressure into the subarachnoid space and quickly spreads through the CSF around the brain and spinal cord.43 Signs and symptoms of ruptured aneurysm include violent headache, stiff neck, photophobia, vomiting, hemiplegia, aphasia, seizure, and CN (III, IV, VI) palsy.17 Management of cerebral aneurysm involves CT scan or angiogram to closely evaluate the aneurysm, followed by aneurysm clipping, embolization, coiling, or balloon occlusion Subarachnoid Hemorrhage Subarachnoid hemorrhage, the accumulation of blood in the subarachnoid space, is most commonly the result of aneurysm rupture, or less commonly a complication of AVM, tumor, infection, or trauma It is graded from I to V according to the Hunt and Hess scale (Table 6-24).17,65 SAH is diagnosed by history, clinical examination, noncontrast CT scan, LP, or angiogram The management of SAH depends on its severity and may include surgical aneurysm repair with blood evacuation; ventriculostomy; and supportive measures to maximize neurologic, cardiac, and respiratory status, rehydration, and fluid-electrolyte balance Complications of SAH include rebleeding, hyponatremia, hydrocephalus, seizure, and vasospasm Vasospasm is the spasm (constriction) of one or more cerebral arteries that occurs to 12 days after SAH.66 The etiology is unknown and is diagnosed II III IV V 147 Asymptomatic, mild headache and mild nuchal rigidity, no neurologic deficit Moderate to severe headache, nuchal rigidity, without neurologic deficit other than cranial nerve palsy Drowsiness, confusion, with mild focal neurologic deficit Stupor, moderate to severe focal deficits, such as hemiplegia Comatose, decerebrate posturing Adapted from Daroff RB, Fenichel GM, Jankovic J et al, editors: Bradley’s neurology in clinical practice, ed 6, Philadelphia, 2012, Saunders, p 1078 by either transcranial Doppler, cerebral angiography, or CT Vasospasm results in cerebral ischemia distal to the area of spasm if untreated The signs and symptoms of vasospasm are worsening level of consciousness, agitation, decreased strength, altered speech, pupil changes, headache, and vomiting, and they may wax and wane with the degree of vasospasm There is currently a vast amount of research concerning treatment of vasospasm HHH therapy (hypertension, hypervolemia, and hemodilution) has traditionally been the treatment of choice for vasospasm66; however, recent studies have questioned the validity of hemodilution as an effective strategy.67,68 Additional treatment options being studied include angioplasty69,70 and administration of intra-arterial medicines such as calcium channel blockers71 or inotropes, specifically milrinone.72 Dementia Dementia is a syndrome of acquired persistent dysfunction in several domains of intellectual function including memory, language, visuospatial ability, and cognition (abstraction, mathematics, judgment, and problem solving).73 There are numerous conditions that can cause or contribute to dementia, including: • Alzheimer’s disease • Acquired immunodeficiency syndrome • Alcoholism • Lewy body dementia • Metabolic disorders • Multi-infarct dementia • Multiple sclerosis • Neoplasms • Parkinson’s disease • Vascular dementia It is beyond the scope of this book to discuss each type in depth The following are some of the most common dementias encountered in the acute care setting Alzheimer’s disease (AD) is the most common cause of dementia.73 Patients with AD usually experience a gradual onset of cognitive deficits caused by amyloid plaques in the brain that replace healthy white matter There is no specific test for diagnosis A detailed medical history, mini–mental exam, neurologic exam, and MRI assist in diagnosing AD In the acute care setting, patients with AD are often admitted with a sudden 148 CHAPTER 6    Nervous System decline in function including decreased interactions with caregivers, decrease in initiation, apraxia, or combative behavior Infections such as urinary tract infection can cause the decline in function, and symptoms usually improve with antibiotics Lewy body dementia (LBD) is characterized by marked fluctuations in cognition, visual and auditory hallucinations, clouding of consciousness, and mild spontaneous extrapyramidal symptoms caused by a pathologic accumulation of Lewy bodies in the brain stem and cortex.73 These patients also display a pronounced sensitivity to antipsychotics, with a tendency to develop severe parkinsonism.74 The diagnosis is made in a similar manner as Alzheimer’s disease and is differentiated from AD by the day-to-day fluctuations and the sensitivity to antipsychotics The disease process is progressive with an average mortality of 12 to 13 years after diagnosis.74 Vascular dementia is usually abrupt in onset and may be a consequence of multiple cortical infarctions, multiple subcortical infarctions (lacunar state), ischemic injury to the deep hemispheric white matter, or a combination of these.73 Diagnosis is made through an accurate history that may include atherosclerosis with myocardial infarction, retinopathy, hypertension, or stroke; EEG; and MRI The patient presents with relative preservation of personality with emotional lability, depression, somatic preoccupation, and nocturnal confusion The focus of physical therapy in the acute care setting for all of these patients is to maximize function while ensuring safety of the patient   CLINICAL TIP Patients with dementia have an elevated fear of falling, which can interfere with mobility It is helpful to stand in front of the patient during transfers so that the patient cannot see the floor Keep instructions functional and simple Reduce stimuli and avoid distractions during treatment by closing the door or pulling the curtain Ventricular Dysfunction Hydrocephalus Hydrocephalus is the acute or gradual accumulation of CSF, causing excessive ventricular dilation and increased ICP CSF permeates through the ventricular walls into brain tissue secondary to a pressure gradient There are two types of hydrocephalus: Noncommunicating (obstructive) hydrocephalus, in which there is an obstruction of CSF flow within the ventricular system There may be thickening of the arachnoid villi or an increased amount or viscosity of CSF This condition may be congenital or acquired, often as the result of aqueduct stenosis, tumor obstruction, abscess, or cyst, or as a complication of neurosurgery.4 Communicating hydrocephalus, in which there is an obstruction in CSF flow as it interfaces with the subarachnoid space This condition can occur with meningitis, after head injury, with SAH, or as a complication of neurosurgery.2 Hydrocephalus may be of acute onset characterized by headache, altered consciousness, decreased upward gaze, and papilledema.11 Management includes treatment of the causative factor if possible, or placement of a ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt Normal-pressure hydrocephalus (NPH) is a type of communicating hydrocephalus without an associated rise in ICP and occurs primarily in the elderly.56 NPH is typically gradual and idiopathic but may be associated with previous meningitis, trauma, or SAH.56 The hallmark triad of NPH is altered mental status (confusion), altered gait (usually wide-based and shuffling with difficulty initiating ambulation), and urinary incontinence NPH is diagnosed by history, CT scan, or MRI to document ventriculomegaly, and lumbar puncture LP is performed to remove excessive CSF (usually 40 to 50 ml).56 A video recording is often made of the patient before and after the lumbar puncture to observe for improvements in gait and cognition If symptoms are significantly improved, the decision may be made for VP shunt placement Recent studies have shown up to a 90% success rate in shunt placement in patients who showed improvement after lumbar puncture.75   CLINICAL TIP The clinician should be aware that patients with NPH often present with a similar gait pattern to patients with Parkinson’s disease Cerebrospinal Fluid Leak A CSF leak is the abnormal discharge of CSF from a scalp wound, the nose (rhinorrhea), or the ear (otorrhea) as a result of a meningeal tear A CSF leak can occur with anterior fossa or petrous skull fractures or, less commonly, as a complication of neurosurgery With a CSF leak, the patient becomes at risk for meningitis with the altered integrity of the dura A CSF leak, which usually resolves spontaneously in to 10 days,17 is diagnosed by clinical history, CT cisternography, and testing of fluid from the leak site If the fluid is CSF (and not another fluid [e.g., mucus]), it will test positive for glucose The patient may also complain of a salty taste in the mouth Management of CSF leak includes prophylactic antibiotics (controversial), lumbar drainage for leaks persisting more than days, dural repair for leaks persisting more than 10 days, or VP or VA shunt placement.64   CLINICAL TIP If it is known that a patient has a CSF leak, the therapist should be aware of vital sign or position restrictions before physical therapy intervention If a CSF leak increases or a new leak occurs during physical therapy intervention, the therapist should stop the treatment, loosely cover the leaking area, and notify the nurse immediately CHAPTER 6    Nervous System Seizure A seizure is defined as abnormal neurologic functioning caused by abnormally excessive activation of neurons, either in the cerebral cortex or in the deep limbic system.59 The signs and symptoms of the seizure depend on the seizure locus on the cortex (e.g., visual hallucinations accompany an occipital cortex locus) Seizures can occur as a complication of CVA, head trauma, brain tumor, meningitis, or surgery Febrile state, hypoxia, hyperglycemia or hypoglycemia, hyponatremia, severe uremic or hepatic encephalopathy, drug overdose, and drug or alcohol withdrawal are also associated with seizures.76 Seizures are classified as partial (originating in a focal region of one hemisphere) or generalized (originating in both hemispheres or from a deep midline focus) (Table 6-25) Seizures are of acute onset, with or without any of the following: aura, tremor, paresthesia, sensation of fear, gustatory hallucinations, lightheadedness, and visual changes Seizure history, including prodrome or aura (if any), for the patient with a recent seizure or epilepsy should be established by either chart review or interview to be as prepared as possible to assist the patient if seizure activity should occur Seizure activity can be irrefutably identified only by EEG Synchronized EEG with video recording may be required to differentiate pseudoseizures (also called psychogenic seizures) from seizures, and both may coexist in the same patient.59 Medical management of seizures involves the treatment of causative factors (if possible) and antiepileptic drugs Surgical management for seizure refractory to medical management may consist of the resection of the seizure focus or the implantation of a vagal nerve stimulator.77 Terms related to seizure include17,76: • Prodrome: The signs and symptoms (e.g., smells, auditory hallucinations, a sense of déjà vu) that precede a seizure by hours • Aura: The signs and symptoms (as just listed) that precede a seizure by seconds or minutes • Epilepsy or seizure disorder: Refers to recurrent seizures • Status epilepticus: More than 30 minutes of continuous seizure activity or two or more seizures without full recovery 149 of consciousness between seizures Generalized tonic-clonic status epilepticus is a medical emergency marked by the inability to sustain spontaneous ventilation with the potential for hypoxia requiring pharmacologic and life support Often the result of tumor, CNS infection, or drug abuse in adults • Postictal state: The period of time immediately after a seizure characterized by lethargy, confusion, and, in some cases, paralysis This state can last minutes to hours and even days Syncope Syncope is the transient loss of consciousness and postural tone secondary to cerebral hypoperfusion, usually accompanied by bradycardia and hypotension.77 Syncope can be any of the following78: • Cardiogenic syncope, resulting from drug toxicity; dysrhythmias, such as atrioventricular block or supraventricular tachycardia; cardiac tamponade; atrial stenosis; aortic aneurysm; pulmonary hypertension; or pulmonary embolism • Neurologic syncope, resulting from benign positional vertigo, carotid stenosis, cerebral atherosclerosis, seizure, spinal cord lesions, or peripheral neuropathy associated with diabetes mellitus or with degenerative diseases, such as Parkinson’s disease • Metabolic syncope, resulting from hypoglycemia, hyperventilation-induced alkalosis, or hypoadrenalism • Reflexive syncope, resulting from carotid sinus syndrome, pain, emotions, or a vasovagal response after eating, coughing, or defecation • Orthostatic syncope, resulting from the side effects of drugs, volume depletion, or prolonged bed rest The cause of syncope is diagnosed by clinical history, blood work such as hematocrit and blood glucose, electrocardiogram, Holter or continuous-loop event recorder, echocardiogram, or tilt-table testing CT and MRI are performed only if new neurologic deficits are found.78 EEG may be performed to rule out seizure The management of syncope, dependent on the etiology and frequency of the syncopal episode(s), may include treatment of the causative factor; pharmacologic agents, such as TABLE 6-25  Seizure Classifications Classification Type Characteristics Partial seizures76 Simple partial Complex partial Partial evolving to secondary generalization Tonic Tonic-clonic Partial seizures without loss of consciousness Brief loss of consciousness marked by motionless staring Progression to seizure activity in both hemispheres Generalized seizures76 Clonic Atonic Absence Myoclonic Sudden flexor or extensor rigidity Sudden extensor rigidity followed by flexor jerking This type of seizure may be accompanied by incontinence or a crying noise owing to rigidity of the truncal muscles Rhythmic jerking muscle movements without an initial tonic phase Loss of muscle tone Very brief period (seconds) of unresponsiveness with blank staring and the inability to complete any activity at the time of the seizure Local or gross rapid, nonrhythmic jerking movements 150 CHAPTER 6    Nervous System beta-adrenergic blockers; fluid repletion; or cardiac pacemaker placement Compression stockings, an abdominal binder, slowly raising the head of the bed before sitting at the edge of the bed, and lower extremity exercises once sitting can help to reduce orthostatic hypotension Neuroinfectious Diseases Refer to Chapter 13 for a description of encephalitis, meningitis, and poliomyelitis Vestibular Dysfunction Dizziness is one of the leading complaints of patients seeking medical attention It is up to the clinician to take a detailed history of the complaint to determine the primary etiology Patients use the term dizzy to describe a multitude of symptoms: • Vertigo: A sense that the environment is moving or spinning (usually caused by vestibular dysfunction) • Lightheadedness: A feeling of faintness (usually caused by orthostatic hypotension, hypoglycemia, or cardiac in origin; refer to Chapters and for further details) • Dysequilibrium: Sensation of being off balance (usually associated with lower extremity weakness or decreased proprioception caused by neuropathy) Vertigo is the hallmark symptom of vestibular dysfunction The vestibular system is complex and made up of a peripheral system and a central system The peripheral system includes three semicircular canals and two otolith organs in the inner ear The central system includes pathways between the inner ear, the vestibular nuclei in the brainstem, cerebellum, cerebral cortex, and the spinal cord The vestibular system functions to: • Stabilize visual images on the retina during head movement for clear vision • Maintain postural stability during head movements • Maintain spatial orientation After the clinician has determined that there is a vestibular system pathology (Table 6-26), the next step is to determine if the pathology is peripheral or central (Table 6-27) Peripheral vestibular system pathology includes benign positional paroxysmal vertigo (BPPV), acute vestibular neuronitis, Ménière’s disease, and ototoxicity These conditions are discussed next Central vestibular pathology is caused by stroke affecting the cerebellar supply and/or vertebral artery; TIA; traumatic brain injury; migraine; tumor; and demyelinating diseases such as MS that affect the eighth cranial nerve.7,79,80 The underlying cause of the pathology must be treated for optimal recovery Physical therapy focuses on the primary diagnosis and compensatory strategies to help with nystagmus or unresolved vertigo Benign Positional Paroxysmal Vertigo BPPV, the most common peripheral vestibular disorder,79 is characterized by severe vertigo associated with specific changes in head position with or without nausea and vomiting The impairments are directly caused by a misplaced otoconium in the semicircular canal from head trauma, whiplash injury, surgery, prolonged inactivity, or aging.9 The otoconia are either “free-floating” in the canal, giving rise to canalithiasis, or adhered to the cupola in the canal, called cupulolithiasis Typically, symptoms of vertigo last less than 60 seconds7 and are precipitated by specific head movements such as looking up to a high shelf, rolling over in bed to one direction, or lying on a specific side The Hallpike-Dix test (Figure 6-9) is the most common test for BPPV and is performed in the following manner79: The patient is positioned on an examination table such that when he or she is placed supine, the head extends over the edge The patient is lowered quickly with the head supported and turned 45 degrees to one side or the other The eyes are carefully observed If no abnormal eye movements are seen in a 30-second time period, the patient is returned to the upright position The maneuver is repeated with the head turned in the opposite direction The direction, duration, and time of onset of the nystagmus is noted and is helpful in determining which semicircular canal is involved as well as differentiating between canalithiasis and cupulolithiasis In canalithiasis, onset of symptoms will be delayed to 20 seconds and will last less than 40 FIGURE 6-9  Hallpike-Dix maneuver for eliciting nystagmus and vertigo due to posterior or anterior canal BPPV The patient’s head is first turned 45 degrees to the right The patient’s neck and shoulders are then brought into the supine position with the neck extended below the level of the examination table The patient is observed for nystagmus or complaints of vertigo The patient is next returned to the upright position if the test is negative (From Herdman S: Treatment of benign paroxysmal positional vertigo, Phys Ther 70:381-388,1990.) CHAPTER 6    Nervous System 151 TABLE 6-26  Tests and Measures for Vestibular Dysfunction* Test Test Procedure Vestibular Pathology Static ocular observation The eyes are examined for the presence of nystagmus while the head is still If nystagmus is present, the clinician observes for any change with gaze fixation Saccades are examined by asking the patient to alternately fixate (with the head still) the examiner’s nose and then finger, held at different locations at approximately 15 degrees away from primary position The velocity, accuracy, and initiation time are observed The patient fixates on a close object (examiner’s nose) while the head is manually rotated, by the examiner, in an unpredictable direction using a small-amplitude, high-acceleration angular thrust The patient closes his or her eyes while the examiner flexes the head 30 degrees and oscillates the head horizontally for 20 cycles at a frequency of reps per second Once the oscillations are stopped, the patient opens his or her eyes and the examiner observes for nystagmus The patient’s head is rotated 45 degrees to one side in sitting and moved into a supine position with the head extended 30 degrees over the end of the examination table with the head still rotated The examiner observes for the presence of nystagmus The patient attempts to read the lowest line of an eye chart while the clinician horizontally oscillates the patient’s head at a frequency of reps per second Air or water is infused into the external auditory canal The change in temperature generates nystagmus within the horizontal SCC in intact vestibular systems Patients are rotated in a chair in the dark Nystagmus is present in intact vestibular systems Patient stands with the feet together with eyes open and then with the eyes closed There are six parts to the test: In condition 1, the patient stands on a fixed platform with eyes open In 2, the patient stands on a fixed platform with the eyes closed In 3, the patient stands on a fixed platform with moving vision screen In conditions 1-3, the patient is relying on somatosensory and vestibular input The test is repeated with a moving platform to distort somatosensory input, and in condition (moving platform and moving vision screen), the patient is relying on vestibular input alone Sway is noted and recorded as minimal, mild or moderate, and fall Nystagmus is present when the head is still and improves with gaze fixation indicative of unilateral vestibular hypofunction Examination of saccades Head thrust test Head-shaking–induced nystagmus Hallpike-Dix test Dynamic visual acuity (DVA) test Caloric testing Rotary chair test Rhomberg test Sensory organization test Slowed saccades or the inability to complete without also moving the head indicates vestibular pathology The eyes will not move as quickly as the head rotation, and the eyes move off the target with a corrective saccade to reposition the eyes on the target This is indicative of vestibular hypofunction Horizontal nystagmus indicates a unilateral peripheral vestibular lesion, with the slow phase of nystagmus toward the side of the lesion Vertical nystagmus suggests a central lesion The presence of nystagmus indicates BPPV A decrement in visual acuity of three or more lines during the head movement indicates vestibular hypofunction The absence of or slowed nystagmus indicates pathology in the horizontal SCC The absence of or slowed nystagmus indicates pathology in the horizontal SCC Increase in sway or loss of balance with the eyes closed may indicate vestibular dysfunction The patient will be unable to maintain balance in condition if vestibular dysfunction is present and vision and somatosensory input are intact The examiner has to be aware that patients may also lose their balance in other conditions because of impaired vision or sensation that is seen normally in the aging process Data from O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation, ed 5, Philadelphia, 2007, FA Davis; Cummings CW, Flint PW et al, editors: Otolaryngology: head & neck surgery, ed 4, Philadelphia, 2005, Mosby BPPV, Benign positional paroxysmal vertigo; SCC, semicircular canal *Before performing these tests, ensure that the patient’s cervical spine is intact and can tolerate neck/head rotation Also ensure that the vertebral arteries are not compromised 152 CHAPTER 6    Nervous System TABLE 6-27  Symptoms Associated with Peripheral versus Central Vestibular Pathology Symptom Peripheral Central Balance deficits Hearing loss Mild to moderate Accompanied with fullness of the ears and tinnitus Unidirectional in all gaze positions; decreases with visual fixation Can be severe Usually not present Severe, ataxia usually present Rare; if it does occur, often sudden and permanent Nystagmus Nausea Additional neurologic impairment Changes direction in different gaze positions; no change with visual fixation Variable, may be absent Can include diplopia, altered consciousness, lateropulsion Data from Cummings CW et al, editors: Otolaryngology: head & neck surgery, ed 4, Philadelphia, 2005, Mosby; Schubert MC: Vestibular disorders In O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation, ed 5, Philadelphia, 2007, FA Davis, p 1013 A C B D FIGURE 6-10  The Epley maneuver (From Furman JM, Cass SP: Benign paroxysmal positional vertigo, N Engl J Med 341:1590-1596, 1999 Copyright 1999 Massachusetts Medical Society All rights reserved.) seconds.81 In cupulolithiasis, onset of symptoms is immediate and continues for more than 60 seconds If the Hallpike-Dix test is positive for canalithiasis, the Epley maneuver (Figure 6-10) is utilized to reposition the otoconia by sequentially moving the head into four positions, staying in each position for roughly as long as the nystagmus lasted during the Hallpike-Dix test For example, if the nystagmus lasted for 25 seconds during the Hallpike-Dix test, each position during the Epley maneuver is held for 25 seconds Of cases of BPPV, 95% are posterior canalithiasis and can be treated with the Epley maneuver Treatment of cupulolithiasis and horizontal canalithiasis are beyond the scope of this book The reader is encouraged to refer to Susan Herdman’s Vestibular Rehabilitation, ed 3, for more information The recurrence rate for BPPV after these maneuvers is about 30% at year, and in some instances a second treatment may be necessary.81 Physical Therapy Implications.  • Contraindications for the Hallpike-Dix test and Epley maneuver include vertebral artery stenosis, cervical spine dysfunction, or osteoporosis • Recommend discussing with the physician whether premedicating the patient with meclizine before performing the Epley or Hallpike-Dix maneuvers is appropriate It may help to reduce or eliminate nausea/vomiting from the maneuvers • The clinician should direct the patient to keep his/her chin tucked to the shoulder (closest to the ground) when transitioning from the last position of the Epley maneuver to sitting, to avoid the otoconia dropping into the horizontal canal Acute Vestibular Neuronitis Acute vestibular neuronitis (vestibular neuritis) is an inflammation of the vestibular nerve, usually caused by viral infection.80 Symptoms include a dramatic, sudden onset of vertigo lasting days, with gradual improvement Nystagmus may or may not be present, and hearing deficits are not noted Treatment is usually supportive, and symptoms should resolve in to weeks Treatment with antivirals has not been shown to be effective.82 Vestibular neuritis can be mistaken for BPPV A detailed history can usually differentiate between these two disorders before the patient is examined In cases of neuritis, the patient usually can tell the examiner in vivid detail what they were doing at the sudden onset of dizziness Dizziness is constant and usually associated with nausea and vomiting With BPPV, symptoms usually are provoked by a change in position or specific head movement and resolve with rest or gaze stabilization In cases of neuritis, patients should be encouraged to keep well hydrated and to sit out of bed, in a supportive chair and well-lit room, to maximize somatosensory and visual input Ménière’s Disease Ménière’s disease (idiopathic endolymphatic hydrops) is a disorder of the inner ear associated with spontaneous, episodic attacks of vertigo; sensorineural hearing loss that usually fluctuates; tinnitus; and often a sensation of aural fullness.79 This is likely caused by an increase in endolymphatic fluid causing distention of the membranous labyrinth.9 Ménière’s disease is usually treated with a salt-restricted diet and the use of diuretics to control the fluid balance within the ear as well as vestibular suppressing medications such as meclizine When conservative treatment has failed, an endolymphatic shunt can be placed; ablation of a portion of the labyrinth can be attempted; or vestibular neurectomy can be performed Physical therapy focuses on patient education and compensatory strategies such as gaze and postural stabilization Bilateral Vestibular Hypofunction Bilateral vestibular hypofunction (BVH) is most commonly caused by ototoxicity of aminoglycosides (gentamicin, streptomycin) The bilateral loss of vestibular function leads to oscillopsia (oscillating or swinging vision) and unsteady gait to varying degrees.79 Impairments are usually permanent, although patients can return to high levels of function by learning to use visual and somatosensory information to make up for the loss of vestibular function Other, less common causes of BVH CHAPTER 6    Nervous System 153 include meningitis, autoimmune disorders, head trauma, tumors on each eighth cranial nerve, TIA of vessels supplying the vestibular system, and sequential unilateral vestibular neuronitis.7 Common Degenerative Central Nervous System Diseases Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, is the progressive degeneration of upper and lower motor neurons, primarily the motor cells of the anterior horn and the corticospinal tract The etiology of ALS is unknown except for familial cases Signs and symptoms of ALS depend on the predominance of upper or lower motor neuron involvement and may include hyperreflexia, muscle atrophy, fasciculation, and weakness, which result in dysarthria, dysphagia, respiratory weakness, and immobility.83 If more upper motor neurons are affected, the symptoms will be primarily clumsiness, stiffness, and fatigue, whereas lower motor neuron degeneration will present as weakness or atrophy and occasionally fasciculations Bulbar symptoms include hoarseness, slurring of speech, choking on liquids, and difficulty initiating swallowing and are more predominant in cases of familial ALS.43 ALS is diagnosed by clinical presentation, EMG, nerve conduction velocity (NCV) studies, muscle and nerve biopsies, and neuroimaging studies to rule out other diagnoses.7 Owing to the progressive nature of ALS, management is typically supportive or palliative, depending on the disease state, and may include pharmacologic therapy (Rilutek [riluzole]), spasticity control, bronchopulmonary hygiene, and nutritional and psychosocial support.64 Physical therapy and rehabilitation are important with patients with ALS to maximize compensatory strategies and to prescribe appropriate adaptive equipment to maintain the patient’s independence for as long as possible Guillain-Barré Syndrome Guillain-Barré syndrome (GBS), or acute inflammatory demyelinating polyradiculopathy, is caused by the breakdown of Schwann cells by antibodies.64 There is an onset of paresthesia, pain (especially of the lumbar spine), symmetric weakness (commonly distal to proximal, including the facial and respiratory musculature), diminishing reflexes, and autonomic dysfunction approximately to weeks after a viral infection GBS is diagnosed by history, clinical presentation, CSF sampling (increased protein level), and EMG studies (which show decreased motor and sensory velocities).84 Once diagnosed, the patient with GBS is hospitalized because of the potential for rapid respiratory muscle paralysis.84 Functional recovery varies from full independence to residual weakness that takes 12 to 24 months to resolve.64,84 GBS is fatal in 5% to 10% of cases.85 The management of GBS may consist of pharmacologic therapy (immunosuppressive agents), plasma exchange, intravenous immunoglobulin, respiratory support, physical therapy, and the supportive treatment of associated symptoms (e.g., pain management) 154 CHAPTER 6    Nervous System BOX 6-1  Definitions and Terminology Used to Describe Categories of Multiple Sclerosis • Relapsing-remitting MS (RRMS): Characterized by relapses with either full recovery or some remaining neurologic signs/ symptoms and residual deficit on recovery; the periods between relapses are characterized by lack of disease progression • Primary-progressive MS (PPMS): Characterized by disease progression from onset, without plateaus or remissions or with occasional plateaus and temporary minor improvements • Secondary-progressive MS (SPMS): Characterized by initial relapsing-remitting course, followed by progression at a variable rate that may also include occasional relapses and minor remissions • Progressive-relapsing MS (PRMS): Characterized by progressive disease from onset but without clear acute relapses that may or may not have some recovery or remission; commonly seen in patients who develop the disease after 40 years of age • Benign MS: Characterized by mild disease in which patients remain fully functional in all neurologic systems 15 years after disease onset • Malignant MS (Marburg’s variant): Characterized by rapid progression leading to significant disability or death within a relatively short time after onset Multiple Sclerosis MS is the demyelination of the white matter of the CNS and of the optic nerve, presumably an autoimmune reaction induced by a viral or other infectious agent.7 Symptoms of MS are highly variable from person to person, and the specific type of MS is categorized by the progression of symptoms (Box 6-1).7 MS typically occurs in 20 to 40 year olds and in women more than in men It is diagnosed by history (onset of symptoms must occur and resolve more than once), clinical presentation, CSF sampling (increased myelin protein and immunoglobulin G levels, called oligoclonal bands), evoked potential recording, and MRI (which shows the presence of two or more plaques of the CNS).7,11 These plaques are located at areas of demyelination where lymphocytic and plasma infiltration and gliosis have occurred Signs and symptoms of the early stages of MS may include focal weakness, fatigue, diplopia, blurred vision, equilibrium loss (vertigo), paresthesias, Lhermitte’s sign, and urinary incontinence Additional signs and symptoms of the later stages of MS may include ataxia, paresthesias, spasticity, sensory deficits, hyperreflexia, tremor, and nystagmus.83 The management of MS may include pharmacologic therapy (corticosteroids for   CLINICAL TIP Patients with MS usually present with an adverse reaction to heat, triggering an exacerbation marked by decline in function and an increase in fatigue Heat stressors are anything that can raise body temperature, including sun exposure, hot environment, or a hot bath or pool This exacerbation usually resolves within 24 hours acute relapse/exacerbations; synthetic interferons such as interferon beta-1a [Avonex, Rebif]; or immunosuppressants such as mitoxantrone [Novantrone]), skeletal muscle relaxants (baclofen), physical therapy, and the treatment of associated disease manifestations (e.g., bladder dysfunction) Parkinson’s Disease Parkinson’s disease (PD) is a neurodegenerative disorder caused by a loss of dopaminergic neurons in the substantia nigra, as well as other dopaminergic and nondopaminergic areas of the brain.86 PD is characterized by progressive onset of bradykinesia, altered posture and postural reflexes, resting tremor, and cogwheel rigidity Other signs and symptoms may include shuffling gait characterized by the inability to start or stop, blank facial expression, drooling, decreased speech volume, an inability to perform fine-motor tasks, and dementia.43,83 PD is diagnosed by history, clinical presentation, and MRI (which shows a light rather than dark substantia nigra).11,65 The management of PD mainly includes pharmacologic therapy with antiparkinsonian agents and physical therapy Levodopa is the most effective treatment for PD, but chronic use can cause hallucinations, dyskinesias, and motor fluctuations.43 There are also several surgical options that have emerged including the placement of a deep brain stimulator (DBS) and, most recently, stem cell implants The DBS has showed the most promise, with recent studies showing improvement in quality of life rating87 and a decrease in tremors.88 To date there have been limited studies completed to support the effectiveness of fetal graft transplantation in humans,88 although multiple studies using rat models have showed improvements.89,90   CLINICAL TIP The clinician should be aware that patients with PD, especially those taking a beta blocker, have a higher incidence of orthostatic hypotension and have a tendency toward retropulsion (pushing posteriorly in sitting and standing) with mobility General Management Intracranial and Cerebral Perfusion Pressure The maintenance of normal ICP or the prompt recognition of elevated ICP is one of the primary goals of the team caring for the postcraniosurgical patient or the patient with cerebral trauma, neoplasm, or infection ICP is the pressure CSF exerts within the ventricles This pressure (normally to 15 mm Hg) fluctuates with any systemic condition, body position, or activity that increases cerebral blood flow, blood pressure, or intrathoracic or abdominal pressure; decreases venous return; or increases cerebral metabolism The three dynamic variables within the fixed skull are blood, CSF, and brain tissue As ICP rises, these variables change in an attempt to lower ICP via the following mechanisms: cerebral vasoconstriction, compression of venous sinuses, decreased CSF production, or shift of CSF to the subarachnoid space When CHAPTER 6    Nervous System 155 TABLE 6-28  Early and Late Signs of Increased Intracranial Pressure Observation Early Late Level of consciousness Confusion, restlessness, lethargy Ipsilateral pupil sluggish to light, ovoid in shape, with gradual dilatation Coma Pupil appearance A Vision Motor B FIGURE 6-11  Herniation syndromes depicted Intracranial shifts from supratentorial lesions A, Normal location of structures B, Various herniation syndromes are demonstrated: 1, Cingulate gyrus herniating under falx cerebri 2, Temporal lobe herniating downward through the tentorial notch 3, Compression of contralateral cerebral peduncle 4, Downward displacement of brain stem through tentorial notch showing central herniation syndrome (From Beare PG, Myers JL, editors: Adult health nursing, ed 3, Philadelphia, 1998, Saunders, p 919.) these compensations fail, compression of brain structures occurs, and fatal brain herniation will develop if untreated (Figure 6-11) The signs and symptoms of increased ICP are listed in Table 6-28 The methods of controlling ICP, based on clinical neurologic examination and diagnostic tests, are outlined in Table 6-29 Table 18-5 describes the different types of ICP monitoring systems Cerebral perfusion pressure (CPP), or cerebral blood pressure, is mean arterial pressure minus ICP It indicates oxygen delivery to the brain Normal CPP is 70 to 100 mm Hg CPPs at or less than 60 mm Hg for a prolonged length of time correlate with ischemia and anoxic brain injury.91 The following are terms related to ICP: • Brain herniation: The displacement of brain parenchyma through an anatomic opening; named according to the location of the displaced structure (e.g., transtentorial herniation is the herniation of the cerebral hemispheres, diencephalon, or midbrain beneath the tentorium cerebelli) • Mass effect: The combination of midline shift, third ventricle compression, and hydrocephalus.11 Blurred vision, diplopia, and decreased visual acuity Contralateral paresis Vital signs Stable blood pressure and heart rate Additional findings Headache, seizure, cranial nerve palsy Papilledema, ipsilateral pupil dilated and fixed, or bilateral pupils dilated and fixed (if brain herniation has occurred) Same as early signs but more exaggerated Abnormal posturing, bilateral flaccidity if herniation has occurred Hypertension, bradycardia, and altered respiratory pattern (Cushing’s triad); increased temperature Headache, vomiting, altered brain stem reflexes Data from Hickey JV: The clinical practice of neurological and neurosurgical nursing, ed 4, Philadelphia, 1997, Lippincott • Midline shift: The lateral displacement of the falx cerebri secondary to a space-occupying lesion • Space-occupying lesion: A mass lesion, such as a tumor or hematoma that displaces brain parenchyma and may result in the elevation of ICP and shifting of the brain Another primary goal of the team is to prevent further neurologic impairment The main components of management of the patient with neurologic dysfunction in the acute care setting include pharmacologic therapy, surgical procedures, and physical therapy intervention Pharmacologic Therapy A multitude of pharmacologic agents can be prescribed for the patient with neurologic dysfunction These include antianxiety medications (see Chapter 19, Table 19-15), anticonvulsants (see Chapter 19, Table 19-16), antidepressants (see Chapter 19, Table 19-17), antipsychotics (see Chapter 19, Table 19-18), mood stabilizers (see Chapter 19, Table 19-19), Parkinson’s medications (see Chapter 19, Table 19-21), diuretics (see Chapter 19, Table 19-3), and adrenocorticosteroids (see Chapter 19, Table 19-8) Additional pharmacologic agents for medical needs include antibiotics (e.g., for infection or after neurosurgery), antihypertensives, thrombolytics, anticoagulants, chemotherapy and 156 CHAPTER 6    Nervous System TABLE 6-29  Treatment Options to Decrease Intracranial Pressure (ICP) Variable Treatment Blood pressure Inotropic drugs to maintain mean arterial pressure > 90 mm Hg to aid in cerebral perfusion, or antihypertensives Osmotic diuretic to minimize cerebral edema Normocapnia* to maximize cerebral oxygen delivery by limiting cerebral ischemia from the vasoconstrictive effects of decreased Paco2 Ventriculostomy to remove cerebrospinal fluid Barbiturates to decrease cerebral blood flow or other medication to decrease the stress of noxious activities Head of the bed positioned at 30-45 degrees to increase cerebral venous drainage Promote neutral cervical spine and head position Dim lights, decreased noise, frequent rest periods to decrease external stimulation Prophylactic anticonvulsant medication Normothermia or induced hypothermia to 32-35° C (e.g., cooling blanket or decreased room temperature) to decrease cerebral metabolism Osmotherapy Mechanical ventilation Cerebrospinal fluid drainage Sedation/paralysis Positioning Environment Seizure control Temperature control Data from Wong F: Prevention of secondary brain injury, Crit Care Nurs 20:18-27, 2000 *Routine aggressive hyperventilation is no longer used for the control of elevated ICP Hyperventilation can contribute to secondary brain injury because of a rebound increase in cerebral blood flow and volume in response to a decreased cerebrospinal fluid pH TABLE 6-30  Common Neurosurgery Procedures Aneurysm clipping Burr hole Craniectomy Cranioplasty Craniotomy Embolization Evacuation Shunt placement Stereotaxis The obliteration of an aneurysm with a surgical clip placed at the stem of the aneurysm A small hole made in the skull with a drill for access to the brain for the placement of ICP monitoring systems, hematoma evacuation, or stereotactic procedures; a series of burr holes is made before a craniotomy The removal of incised bone, usually for brain (bone flap) tissue decompression; the bone may be permanently removed or placed in the bone bank or temporarily placed in the subcutaneous tissue of the abdomen (to maintain blood supply) and replaced at a later date The reconstruction of the skull with a bone graft or acrylic material to restore the protective properties of the scalp and for cosmesis An incision through the skull for access to the brain for extensive intracranial neurosurgery, such as aneurysm or AVM repair or tumor removal; craniotomy is named according to the area of the bone affected (e.g., frontal, bifrontal, frontotemporal [pterional], temporal, occipital) The use of arterial catheterization (entrance usually at the femoral artery) to place a material, such as a detachable coil, balloon, or sponge, to clot off an AVM or aneurysm The removal of an epidural, subdural, or intraparenchymal hematoma via burr hole or craniotomy The insertion of a shunt system that connects the ventricular system with the right atrium (VA shunt) or peritoneal cavity (VP shunt) to allow the drainage of CSF when ICP rises The use of a stereotactic frame (a frame that temporarily attaches to the patient’s head) in conjunction with head CT results to specifically localize a pretargeted site, as in tumor biopsy; a burr hole is then made for access to the brain AVM, Arteriovenous malformation; CSF, cerebrospinal fluid; CT, computed tomography; ICP, intracranial pressure; VA, ventriculoatrial; VP, ventriculoperitoneal radiation for CNS neoplasm, stress ulcer prophylaxis (e.g., after SCI), pain control, and neuromuscular blockade Neurosurgical Procedures The most common surgical and nonsurgical neurologic procedures are described in Table 6-30 Refer to Table 5-3 for a description of surgical spine procedures and Table 18-5 for a description of ICP monitoring devices The clinician should pay close attention to head-of-bed positioning restrictions for the patient who has recently had neurosurgery Often, the head of the bed is at 30 degrees, or it may be flat for an initial 24 hours and then gradually elevated 15 to 30 degrees per day depending on the location of surgery (supratentorial or infratentorial, respectively).17   CLINICAL TIP The physical therapist should be aware of the location of a craniectomy because the patient should not have direct pressure applied to that area Look for signs posted at the patient’s bedside that communicate positioning restrictions Physical Therapy Intervention Goals The primary physical therapy goals in treating patients with primary neurologic pathology in the acute care setting include maximizing independence and promoting safety with gross functional activity Another main goal is to assist in the prevention of the secondary manifestations of neurologic dysfunction and immobility, such as pressure sores, joint contracture, and the deleterious effects of bed rest (see Chapter 1, Table 1-1) Management Concepts for Patients with Neurologic Dysfunction • A basic understanding of neurologic pathophysiology is necessary to create appropriate functional goals for the patient The therapist must appreciate the difference between reversible and irreversible and between nonprogressive and progressive disease states • There are a number of natural changes of the nervous system with aging, such as decreased coordination, reflexes, balance, and visual acuity Be sure to accommodate for these normal changes in the examination of and interaction with the elderly patient • Take extra time to observe and assess the patient with neurologic dysfunction, as changes in neurologic status are often very subtle CHAPTER 6    Nervous System 157 • A basic knowledge of the factors that affect ICP and the ability to modify treatment techniques or conditions during physical therapy intervention for the patient with head trauma, after intracranial surgery, or other pathology interfering with intracranial dynamics is necessary for patient safety • Patient and family or caregiver education is an important component of physical therapy Incorporate information about risk factor reduction (e.g., stroke prevention) and reinforce health care team recommendations (e.g., swallowing strategies per the speech-language pathologist) • There are a variety of therapeutic techniques and motorcontrol theories for the treatment of the patient with neurologic dysfunction Do not hesitate to experiment with or combine techniques from different schools of thought • Be persistent with patients who not readily respond to typical treatment techniques because these patients most likely present with perceptual impairments superimposed on motor and sensory deficits • Recognize that it is rarely possible to address all of the patient’s impairments at once; therefore, prioritize the plan of care according to present physiologic status and future 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APPENDIX 6A  MODIFIED TARDIEU SCALE SCORING SHEET Date/Time Joint/Muscle Position of Patient Velocity (V) Muscle Response (X) Angle of Catch (Y) Example of a completed scoring sheet: Date/Time Joint/Muscle Position of Patient 7/5/2012 8:15 am Hamstring Supine with the hip flexed to 90° 7/7/2012 8:20 am (after Botox injection) Hamstring Supine with the hip flexed to 90° Velocity (V) Muscle Response (X) V1 Angle of Catch (Y) N/A V2 −50° of extension V3 −60° of extension V1 N/A V2 N/A V3 −30° of extension As you can see, this is a more objective way of measuring spasticity, and trends can be more easily identified ... white matter and provides the pathway for the ascending and descending tracts, as shown in cross-section in Figure 6- 5 and outlined in Table 6- 6 TABLE 6- 6  Major Ascending and Descending White... speech? CHAPTER 6    Nervous System 131 FIGURE 6- 6  Dermatome chart based on embryologic segments (From Maitland GD, editor: Vertebral manipulation, ed 5, Oxford, UK, 19 86, Butterworth-Heinemann,... advantages, and disadvantages For the purposes of this text, only the procedures most commonly used in the acute care setting are described CHAPTER 6    Nervous System 139 TABLE 6- 16 Sensation Testing