PERIPHERAL NERVES (CONT’D) More dista esion usua y at media base of pa m Affects intrinsic hand musc es on y Motor: weakness of finger adduction, abduction and thumb adduction (Froment’s sign), c aw-hand and interosseous atrophy Sensory: changes in both dorsa and pa mer surfaces of 4th and 5th fingers May have pain over median proxima forearm (cubita tunne ) Tests: Tine sign positive Motor: weakness of finger adduction and abduction nterosseous atrophy Sensory: changes in pa mer surface of 4th and 5th fingers on y Tests: Tine sign negative Lesion usua y at cubita tunne or u nar groove at the e bow Affects u nar f exor of the wrist, ong f exors of 4th-5th digits and intrinsic hand musc es U nar nerve (C8–T1) Motor: finger drop, wrist re ative y spared Sensory: intact Lesion usua y at the Arcade of Foshse Affects finger and thumb extensors Posterior interosseous branch of radia nerve (C7–8) U nar nerve (C8–T1) Signs and symptoms Motor: weakness of shou der abduction, shou der atrophy Sensory: deficit simi ar to C5 esion Motor: weakness of atera rotation of arm Sensory: intact Motor: winging of the scapu a Sensory: intact Motor: wrist drop, weakness of finger and thumb extensors Sensory: changes in dorsa surface of 1st- atera 4th fingers, dorsa surface of arm/forearm Lesion usua y at spira groove of humerus Affects brachioradia is, triceps, wrist, finger and thumb extensors Lesion usua y at suprascapu ar notch of scapu a Affects supraspinatus and infraspinatus Affects serratus anterior Pathophysiology Lesion usua y near shou der joint Affects de toid and teres minor Radia nerve (C5–T1) Long thoracic nerve (C5–7) Subscapu ar nerve (C5–6) MONONEUROPATHIES Nerve (origin) Axi ary nerve (C5–6) Cyc ist’s pa sy Saturday night pa sy (acute compression) is frequent cause Cheira gia paresthetica (entrapment of superficia branch of radia nerve to dorsum of hand) Comments 330 Peripheral Neuropathy PERIPHERAL NERVES (CONT’D) Peronea nerve (L4–S1) Tibia nerve (L5–S2) Sciatic nerve (L4–S3) Lesion usua y at inguina igament Latera femora cutaneous branch of femora nerve (L2–3) Obturator nerve (L3–4) Lesion usua y at pubis or intrape vic Affects thigh adductors Lesion usua y near sciatic notch Affects hamstring musc es, hip abductor and a musc es be ow the knee Lesion usua y at tarsa tunne or near media ma eo us Affects ca f musc es (proxima y), toe f exor, and other intrinsic foot musc es Lesion usua y at neck of fibu a Affects dorsif exors of toes and foot and evertors of foot Lesion usua y just be ow the e bow Affects ong f exors of thumb and index and midd e fingers Lesion usua y proxima to inguina igament Affects i iopsoas (hip f exor) and quadriceps femoris (knee extensor) Pathophysiology Lesion at carpa tunne Affects abductor po icis brevis, proxima musc es inc ude forearm pronator, ong finger, and thumb f exors Anterior interosseous branch of median nerve (C7–T1) Femora nerve (L2–4) MONONEUROPATHIES Nerve (origin) Median nerve (C6–T1) Motor: weakness of foot eversion and foot drop Sensory: deficit simi ar to L5 esion Motor: buck ing of knee, absent knee jerk, weak anterior thigh musc es with atrophy Obturator nerve (hip adduction) not affected Sensory: changes in atera eg to media ma eo us Motor: intact Sensory: dysesthetic hyperpathia of atera thigh (burning) Motor: weakness of hip adduction Sensory: deficit of media thigh Motor: severe ower eg and hamstring weakness, f foot, difficu ty wa king Sensory: changes in ower eg and foot Motor: weak toe f exors Sensory: pain and numbness of so e Signs and symptoms Motor: weakness, pain, numbness and ting ing over thumb, 2nd and 3rd fingers Sensory: changes in pa mer surface of 1st- atera 4th fingers Tests: square wrist sign, c osed fist sign, F ick sign, Tine sign and Pha en sign Motor: weakness of pinch, pain in vo ar forearm Sensory: intact Cross- eg pa sy Tarsa tunne syndrome Overdose victims Mera gia paresthetica (entrapment of atera cutaneous femora nerve to antero atera aspect of thigh) Post-femora catheterization or pe vic surgery with retroperitonea hematoma, diabetes me itus Comments Carpe tunne syndrome Peripheral Neuropathy 331 332 Muscle Weakness Muscle Weakness DIFFERENTIAL DIAGNOSIS CLINICAL FEATURES INFLAMMATORY MYOPATHY polymyositis, dermatomyositis, inclusion body myositis, juvenile dermatomyositis, vasculitis, overlap syndromes (SLE, scleroderma, rheumatoid arthritis, Sjogren’s) INFECTIOUS MYOPATHY BACTERIAL pyomyositis, Lyme myositis VIRAL influenza, parainfluenza, Coxsackie, HIV, CMV, echovirus, adenovirus, EBV FUNGAL trichinosis, toxoplasmosis DRUG/TOXIC MYOPATHY steroid, alcohol, cocaine, heroin, colchicine, antimalarial, statins, fibrates, penicillamine, zidovudine ENDOCRINE MYOPATHY hypothyroidism, hyperthyroidism, Cushing’s, diabetes, acromegaly METABOLIC MYOPATHY hypokalemia, hypocal cemia, hypophosphatemia, hyponatremia, hyper natremia, disorders of carbohydrate/lipid/purine metabolism NEOPLASTIC MYOPATHY paraneoplastic RHABDOMYOLYSIS DRUGS alcohol, cocaine, statins, neuroleptic malignant syndrome, malignant hyperthermia HYPERACTIVITY seizures, exertion PARASITIC / TRAUMA OPERATION IMMOBILITY NEUROLOGIC MOTOR CORTEX stroke, multiple sclerosis, brain tumor, abscess CORTICOSPINAL TRACT/ANTERIOR HORN CELLS spinal cord injury, vitamin B12 deficiency, ALS, polio, lead SPINAL NERVE ROOTS/PERIPHERAL NERVES Guil lain Barre, myeloma, amyloidosis, diabetes NEUROMUSCULAR JUNCTION myasthenia gravis, botulism, Eaton Lambert, organophosphate poisoning MUSCLES myopathies (see above) Related Topics Critical Illness Weakness (p 89) Dermatomyositis (p 279) Eaton Lambert Syndrome (p 319) Myasthenia Gravis (p 318) APPROACH TO CLINICAL DIAGNOSIS FUNCTIONAL VS TRUE MUSCLE WEAKNESS? if functional, consider cardiopulmonary disease, arthritis, anemia, cachexia from malignancy or chronic disease, depression, deconditioning, fibromyalgia if true muscle weakness, proceed to 2 GENERALIZED VS LOCALIZED MUSCLE WEAKNESS? if generalized, consider myasthenia gravis, long standing periodic paralysis, advanced disuse atrophy from prolonged bed rest, or advanced muscle wasting from malignancy if localized, proceed to 3 ASYMMETRIC VS SYMMETRIC MUSCLE WEAKNESS? if asymmetric, consider disease of central or peripheral nervous system (stroke, spinal cord injury, demyelinating disorders, com pression neuropathy, mononeuropathy/ neuritis), disuse atrophy, myasthenia gravis if symmetric, proceed to 4 DISTAL VS PROXIMAL MUSCLE WEAKNESS? if distal, consider peripheral neuropathy, myasthenia gravis, motor neuron disease if proximal, consider myopathies (see differ ential diagnosis), myasthenia gravis, Duch enne muscular dystrophy MRC MUSCLE STRENGTH GRADING 0=no contraction 1=flicker 2=possible only with gravity eliminated 3=against gravity only 4=power decreased but muscle contraction possi ble against resistance 5=normal power resistance MUSCLE STRENGTH preserved in patients with cachexia despite advanced generalized muscle atro phy In contrast, patients with true muscle weakness due to myopathy generally have normal muscle bulk at time of presentation MUSCLE TENDERNESS usually not associated with one of the causes of true muscle weakness, except for infectious myopathies, certain drug induced myopathies, thyroid myopathy, and inherited metabolic myopathies INVESTIGATIONS BASIC CBCD, lytes, urea, Cr, Ca, Mg, PO4, CK, aldolase, LDH, AST, ALT, ANA, ANCA, HBV/HBC serology, cryoglobulin, RF, TSH LABS 333 Approach to Neuroimaging INVESTIGATIONS (CONT’D) SPECIAL EMG AND NERVE CONDUCTION STUDY SPECIFIC ENTITIES (CONT’D) muscle weakness and atro phy Muscle damage second degree to sepsis and multi system organ failure CRITICAL MYOPATHY MUSCLE BIOPSY / WORKUP anti Jo and 2, anti SRP (signal recognition particle), anti Mi2 POLYMYOSITIS DERMATOMYOSITIS MANAGEMENT REHABILITATION TREAT UNDERLYING CAUSE SPECIFIC ENTITIES CRITICAL ILLNESS NEUROMUSCULAR DISORDERS CRITICAL ILLNESS POLYNEUROPATHY muscle weak ness and atrophy, # deep tendon reflexes, # per ipheral sensation to light touch and pin prick Associated with sepsis, systemic inflammation DELAYED REVERSAL OF NEUROMUSCULAR BLOCKADE non depolarizing neuromuscular blocking agents (pancuronium, vecuronium) in susceptible patients MYOPATHY ASSOCIATED WITH COMBINED USE OF STEROID AND NEUROMUSCULAR BLOCKING AGENT muscle weakness and atrophy, # deep tendon reflexes AMYOTROPHIC LATERAL SCLEROSIS (ALS) PATHOPHYSIOLOGY combined upper and lower motor neuronal degeneration ! spread to involve multiple myotomes in multiple regions (bulbar, cervical, and lumbosacral) No sensory deficit CLINICAL FEATURES upper motor neuron signs (hyperactive reflexes, extensor plantar responses), lower motor neuron signs (muscle weakness, atro phy, and fasciculations) in multiple regions DIAGNOSIS EMG/NCS TREATMENTS antiglutamate agent (riluzole) DROP HEAD SYNDROME persistent head flexion May be due to myasthenia gravis, polymyositis, or amyotrophic dystonia Approach to Neuroimaging APPROACH TO CT HEAD MODALITIES CT HEAD (unenhanced) particularly useful for acute hemorrhage (subarachnoid, subdural, intra cerebral), skull fractures/trauma, meningiomas, and subacute and chronic strokes Also used as initial workup of acute TIA or stroke and other brain tumors although not as sensitive as MRI MRI HEAD particularly useful for evaluation of stroke (acute, subacute, chronic), hemorrhage (sub acute and chronic), white matter lesions (multiple sclerosis), and lesions of the posterior fossa, brain stem, and spinal cord Also useful for most tumors, epilepsy, demyelinating diseases, inflammatory and infectious conditions (e.g HSV encephalitis), degen erative diseases, and congenital abnormalities MRI WITH GADOLINIUM improved differentiation between pathologic and normal tissues (especially T1 relaxation) This increases the sensitivity and specifi city Contrast may also provide physiologic and func tional information in addition to lesion delineation CT/MR ANGIOGRAPHY used for evaluation of occlusive cerebrovascular disease, dissection, and in the detection of intracerebral aneurysms as small as mm in diameter However, cerebral angiogram remains the gold standard CT/MR VENOGRAPHY extremely sensitive and specific in the diagnosis of venous sinus thrombosis BRAIN PARENCHYMA , hypodensity within the parenchyma suggests infarction or fluid Hyperdensity represents either hematoma (hemorrhage) or calcification A hematoma will produce mass effect upon adjacent structures Cal cification will usually be punctate and have no mass effect GRAY–WHITE DIFFERENTIATION the junction of gray matter and white matter adjacent to the cortex and the basal ganglia should be well defined Poor delineation should raise suspicion of cerebral edema if the finding is global or acute infarction if the finding is localized ANY SUSPICIOUS ASYMMETRIC LESIONS MIDLINE SHIFT VENTRICLES AND SUBARACHNOID SPACES (sulci and cisterns) difficulty with visualization of the basal cisterns may indicate increased intracranial pressure and possibly brain herniation Hyperdensity (white) within the subarachnoid spaces and the dependent portions of the ventricles suggests subarachnoid hemorrhage DURA AND SUBDURAL SPACE check for subdural hemorrhage in subdural window (crescent like), espe cially along the edges of the intracranial cavity BONE AND AIR SPACES check for fractures in bone window and fluid in sinuses 334 APPROACH TO CT HEAD (CONT’D) SKIN AND SUBCUTANEOUS TISSUES check for swelling of extracranial soft tissues in subdural window HEAD CT FINDINGS IN THE ELDERLY SMALL VESSEL DISEASE diffuse brain atrophy, hypodense periventricular white matter due to glio sis, and lacunar infarcts within the basal ganglia LARGER VENTRICLES AND SUBARACHNOID SPACES due to brain atrophy FOCAL CALCIFICATION common within the basal ganglia in the elderly and should not be confused with hemorrhage HEAD CT FINDINGS IN STROKE LOCALIZATION the presenting symptoms can help focus evaluation The majority of infarcts involve the Approach to Neuroimaging HEAD CT FINDINGS IN STROKE (CONT’D) MCA territory or subcortical region Early signs of infarction include the following: HYPERDENSE MCA the suspected MCA must be significantly denser than the contralateral MCA or basilar artery / EDEMA OF THE BASAL GANGLIA AND OR INSULAR COR- involved lentiform nucleus will appear hypo dense with indistinct lateral border The insular cortex will appear swollen compared to the tralateral side SULCAL EFFACEMENT the sulci along the cerebral convexity on the involved side will appear smaller than the other side EVOLUTION hypodense lesions may not appear until after 24 h MRI is superior to CT for identifying acute stroke Lesions may become more hypodense over time Old infarcts are very black TEX ... HEAD SYNDROME persistent head flexion May be due to myasthenia gravis, polymyositis, or amyotrophic dystonia Approach to Neuroimaging APPROACH TO CT HEAD MODALITIES CT HEAD (unenhanced) particularly... to L5 esion Motor: buck ing of knee, absent knee jerk, weak anterior thigh musc es with atrophy Obturator nerve (hip adduction) not affected Sensory: changes in atera eg to media ma eo us Motor:... myasthenia gravis, botulism, Eaton Lambert, organophosphate poisoning MUSCLES myopathies (see above) Related Topics Critical Illness Weakness (p 89) Dermatomyositis (p 279) Eaton Lambert Syndrome (p