branches on the dorsum of the foot caused by excessively tight shoes (usually mountain hiking or ski boots), with resulting dysesthesia and hypesthesia. Hypesthesia of the me- dial portion of the distal phalanx of the great toe results from the pressure of arigidshoe in the presence of either hallux valgus or an osteophytic change of the unguicular process. A painful syndrome of the sciatic nerve, the piriformis syndrome, will be de- scribed below (p. ). Injection Palsies Pathologic Anatomy Injections improperly placed into or in the vicinity of a nerve cause an in- tense foreign body reaction around the nerve, leading to dense fibrosis which may penetrate between the nerve fascicles. Clinical Features Weakness develops immediately af- ter injection in about two-thirds of patients, while only one-sixth have immediate pain. In about 10% of cases, the weakness develops only af- ter an interval of hours or even day s. The weakness is at its worst 24– 48 hours after its onset. A causalgia- like pain syndrome may develop and dominate the clinical picture. Causes Injection palsies are most often due to injections into or near the scia tic nerve (less commonly, the gluteal nerves). They usually cause paresis in the muscles supplied by the common peroneal nerve (lateral half of the sci- atic trunk) and are therefore dis- cussed in this section. The occurrence of an injection palsy is largely determined by the site of in- jection rather than by the substance injected, as many different sub- stances can produce harm in this way. In general, intramuscular injections should be avoided unlessabsolutely necessary. Differential Diagnosis An injection into a gluteal artery can cause Nicolau syndrome, in which part of the gluteal musculature be- comes discolored (blue) and may be- come necrotic. Prophylactic Measures: Proper Injection Technique Intragluteal injections should be car- ried out exclusively in the upper outer quadrant of the buttock, and with the needle perpendicular to the body surface, rather than pointing dorsomedially or caudally. If, on in- sertion of the need le or on injection, the patient complains o f shooting, shock-like pain, orevenofpainthat radiates only to theperiphery, the needle should be immediately with- drawn and the injection performed correctly on the other side. Treatment If an injection palsy occurs, prompt surgical exploration is indicated to remove all pockets of injection fluid from the nerve trunk and its vicinity, and for lysis of any adhe- sions that may be present. General Differential Diagnosis of Peroneal Nerve Lesions Syndromes resembling peroneal nerve palsy have many causes. First among these is L4–5 intervertebral disk herniation with L5 root compres- sion, which leads to marked weak- Common Peroneal Nerve 793 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. ness of dorsiflexion of the great toe, and often to sensory loss on the dor- sum of the foot (mimicking a pero- neal nerve palsy). The sensory loss usually extends far up the limb in the L5 dermatome; this, together with back pain, points tothecorrectdiag- nosis. L5 radiculopathy differs from pero- neal nerve palsy on motor examina- tion in that the former may impair hip abduction and foot inversion (= supination), while the latter does not. Many polyneuropathies begin distally in the lower limb and can produce a steppage gait resembling that of pe- roneal nerve palsy. This can be unilat- eral, at least initially, in (vascular) mononeuropathy multiplex (p. ). In advanced HMSN (p. ), weakness re- sembling that of peroneal nerve palsy is accompanied by calf muscle weak- ness and atrophy, loss of the Achilles reflexes, and,rarely,distal sensory deficits. This familial disease also usually causes pes cavus. The muscle weakness and atrophy (without sen- sory deficit) of Steinert’s myotonic dystrophy are usually accompanied by other signs of this autosomal d om- inant inherited disease. Tibialis Anterior Syndrome (Tibial Compartment Syndrome) This syndrome, caused by ischemia of the dorsiflexor muscles of the foot and toes in the anterior compartment of the leg, is often confuse d with a peripheral peroneal nerve palsy. Pathogenesis The condition is duetoischemicne- crosis of the muscles of the anterior compartment of the leg (tibialis ante- rior, extensorhallucis longus, and ex- tensor digitorum longus). This com- partment is sealed on all sides by wallsofboneand connective tissue, so that edematous tissue within it has no room to expand. If ischemia should arise because of thrombosis, embolism, or occlusion of a proximal artery, a vicious circle of edema and vascular compression ensues. The same may occur in association with a tibial fracture or a traumatic or post- operative hematoma within the com- partment, or with overuse of the leg muscles (military marching, football, etc.). Clinical Features There is intense pain, redness, and swelling in the pretibial region. At the same time, dorsiflexion of the foot and toes becomes painful, and com- plete paralysis maydevelop within hours. Concomitant ischemic damage to the deep peroneal nerve, which traverses the compartment, may cause paralysis of theextensordigito- rum brevis and extensor hallucis bre- vis muscles on the dorsal surface of the foot, as well as sensory loss in the first dorsal interosseous space. The superficial peroneal nerve becomes ischemic in some cases as well, as it is sometimes supplied by a branch of the anterior tibial artery. In such cases, there is additional paralysis of the peroneal muscles, with a corre- sponding sensory deficit. Thus, in its early stage, the pattern of weakness in tibial compartment syndrome closely resembles that of common peroneal nerve palsy. A correct differ- ential diagnosis is possible only on the basis of a careful history, the pres- ence of pain in the tibial compart- ment, and the frequent but not in- variable absence of a pulse in the dor- 794 11 Lesions of Individual Peripheral Nerves Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. salis pedis artery.EMGrevealsnoac- tivity in the necrotic muscles (“silent EMG”), but there is still electrical ac- tivity in the neurogenically paretic extensor digitorum brevis and pero- neal muscles. Prognosis Usually only the neurogenic compo- nent of the paralysis can recover spontaneously as the muscles of the anterior compartment of the leg un- dergo fibrosis, retraction, and per- haps calcification. In the later stages, they are as hard as wood, the ankle cannot be plantar flexed beyond 90°, and there is a hammer-toe deformity due to shortening of the extensor hal- lucis longusmuscle. Treatment Early diagnosis is essential, as fasci- otomy (splitting of the anterior crural fascia) must be performed within the first 24 hours to p re- serve the muscles from infarction. The sameholdsforcompartment syndromes at other sites as well. Tibial Nerve Anatomy The tibial nerve arises from the L4–S3 roots, its fibers lying on the medial side of the sciatic trunk. It supplies the plantar flexors of the foot and toes, and allofthesmallmusclesof the foot excepttheextensor digito- rum brevis and extensor hallucis bre- vis. It provides cutaneous sensory in- nervation to the heel and sole of the foot. It also carries many autonomic fibers. Clinical Features Alesionoftheposterior tibial nerve causes paralysis of the plantar flexors of the foot and toe. Even an incom- plete paralysis impairs toe-walking and diminishes the Achilles reflex. In complete paralysis, there is a valgus posture of the foot,becausetheper- onei, innervated by the superficial peroneal nerve, prevail over the para- lyzed invertors. The toes can no lon- ger be spread or maximally flexed. Sensation on the sole of the foot is impaired. Causes The tibial nerve is well protected in the popliteal fossaandisthus rarely injured – e.g., by a gunshot wound. A supracondylar femoral fracture may damage the sciatic trunk or either of its main divisions. Dislocation of the knee injures the tibial nerve much less frequently than the common pe- roneal nerve. A dorsally angulated or dislocated fracture of the proximal portion of the tibial shaft can damage the trunk of the tibial nerve, and pri- mary surgical exploration is justified in such cases. In other cases, sensory changes on the sole of the foot a nd weakness mayonlyappear in the course of fracture healing; as this is likely due to perineural scarring, sur- gical exploration forneurolysisisin- dicated. The same applies to fractures of the distal third of the tibia. Persons in certain occupations requiring con- tinuous pedaling movements (e.g., potters) are at risk of chronic me- chanical injury to both the tibial and the common peroneal nerves, be- Tibial Nerve 795 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. cause of the anatomical relationship of these nerves to the muscles around the kneejoint. Tarsal Tunnel Syndrome Pathogenesis and Clinical Features The tibial nerve and its two branches, the lateral and medial plantar nerves, can be chronically compressed under the flexor retinac- ulum in the region of the medial malleolus. This can occur in the af- termath of an ankle or heel fracture, or merely an ankle sprain, or for no apparent reason. The resulting tarsal tunnel syndrome is characterized by painful paresthesiae of the sole of the foot that are aggrav ated by walk- ing. Physical examination reveals a sensory deficit in the distribution of the plantar nerves, diminished or ab- sent sweating on the s ole of the foot, and weakness of the small muscles of the sole. The toes cannot be maxi- mally spread. Thereisoftentender - ness to palpation over the course of the tibial nerve. There are also cases with painful pa- resthesiae of the sole, aggravated by walking, in which there is no motor deficit. The symptoms can be imme- diately relieved by tibial nerve block with injection of local anesthetic be- hind the medial malleolus, but this is not a specific test. Diagnostic Evaluation The diagnosis can be confirmed by electromyography. Treatment Tarsal tunnel release by division of the flexor retinaculum is justified if the symptoms are distressing and the diagnosis clear. A pannus-like tissue reaction is found, sometimes accompanied by pseudoneuroma formation in the nerve trunk. Metatarsalgia (Morton’s Toe) Pathogenesis This condition is caused by a fusiform pseudoneuroma of a digital nerve just proximal to its division, usually in the third or fourth interdigital space. Chronic pressure from themetatarsal head on the nerve is the cause. Clinical Features Patients complain of neuralgic, often burning paininthesoleofthefoot, usually in the region of the third and fourth metatarsal heads and the cor- responding two toes. The pain first appears when the patient walks but later becomes continuous and may radiate pro ximally. The pains are of- ten incorrectly attributed to a splay- foot (valgus) deformity. On physical examination, intense pain can be pro- vokedbypressure on the sole of the foot, or by pressing the metatarsal heads on either side of the lesion against each other. The diagnosis is confirmed by the cessation of pain on infiltration of local anesthetic at the site of division of the plantar nerve in the third or fourth interdigital space. The approach is from the dorsum of the foot. Treatment Adequate relief can be obtained in mild cases with special shoes, or foot supports within the shoes, that hold up the arch of the foot just be- hind the metatarsal heads. If the pain persists, the lesion can be excised. 796 11 Lesions of Individual Peripheral Nerves Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. 12 Headache and Facial Pain Overview: Headache and facial pain are due to the irritation of sensitive structures in these regions, among them the major vessels of the base of the brain, por- tions of the basal dura and pia mater, the cerebral venous sinuses, and the cranial nerves that have a sensory component, as well as all extracranial structures. The brain itself is not sensitive to noxious stimuli. Headache and facial pain are sometimes due to a specific disease involving the cranial structures, but are more often the expression of idiopathic disturbances of vasomotor orneuralregulation,in which case no anatomical abnormality of these structures can be found. Table 12.1 Headache history Family history of headache? How long have headaches been pre- sent? Nature of headache: Site? Continuous or episodic? Timing of onset? Speed of development? Nature of pain? Precipitating factors? Duration of episodes? Accompanying signs? Frequency? Headache-free intervals? Intensity? Impairment of activities at home and at work? Treatment/ medication(s) used: Frequency Dose Efficacy Neurologic abnormalities between headache episodes Memory? Neurologic/neuropsychological defi- cits? Epileptic seizures? General symptoms (fatigue, weight gain, circulatory problems, etc.)? Personality Character? Occupation? Private life? Conflicts? Alcohol, tobacco, caffeine, drugs of abuse? Medications? Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. General Aspects History-Taking from Patients with Headache Athoroughandpreciseheadache his- tory often suffices to lead the clini- cian to the correct etiologic diagnosis. The aspects of headache that should be asked about specifically are listed in Table 12.1.Itisalsoimportantto assess the degree to which the head- ache impairs the patient’s functioning in everyday life – e.g., with the Mi- graine Disability Assessment Scale (MIDAS; Table 12.2)(590a,910a). Classification of Headache and Facial Pain Asampleetiologic classification is shown in Table 12.3.Theveryexten- sive table o f the International Head- ache Society is reproduced in abbre- viated form in Table 12.4;theoriginal also contains specific criteria for each diagnosis, and is mainly of use in clin- ical research. Table 12.9,attheendof this chapter, contains a list of the var- ious headache and facial pain syn- dromes according to their clinical fea- tures and localization, as an aid to dif- ferential diagnosis. Table 12.2 Migraine Disability Assessment Scale (MIDAS) questions (590a) Question Days (n) 1Onhowmanydaysinthe last 3 months did you miss work or school because of your headaches? 2Howmanydaysinthelast 3 months was yourproductivity at work or school reduced by half or more because of your head- aches? (Do not include days you counted in question 1 where you missed work or school) 3Onhowmanydaysin the last 3 months did you not do household work because of your headaches? 4Howmanydaysinthelast 3 months was yourproductivity in household work reduced by half or more because of your headaches? (Do not include days you counted in question 3 where you did no household work) 5Onhowmanydaysinthe last 3 months did you miss family, social or leisure activities because of your headaches? Total days (n) Disability: 0–5 Noneormild 6–10 Mild 11–20 Moderate 21 Severe 798 12 Headache and Facial Pain Mumenthaler, Neurology © 2004 Thieme All rights reserved. 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Table 12.3 Classification of the major headache and facial pain syndromes by etiology Primary headache: Tension headache True migraine –Ophthalmicmigraine –Migraine accompagn´ee –Ophthalmoplegic migraine –Abdominal migraine –Basilarmigraine –Dysphrenic migraine Cluster headache (erythroprosopal- gia, Horton’s neuralgia) Rarer forms: –“Ice-cream headache” –Acutepostcoital headache –Carotidynia –Coughheadache –Hemicrania continua –Hypnicheadache Headache in organic vascular disease: Ischemic stroke Hemorrhagic stroke Subarachnoid hemorrhage Cranial (temporal) arteritis Carotid or vertebral artery dissection Headache due to an intracranial mass: Brain tumor Subdural hematoma Brain abscess Headache due to impaired CSF circulation: Obstruction to CSF flow CSF malresorption Intracranial hypotension Spondylogenic headache: Cervical spondylosis Cervical migraine Whiplash injury Tension headache (“psychogenic” headache) Other “non-neurological” causes of headache: Arterial hypertension Intracranial inflammatory/infectious processes Toxic and iatrogenic headache ENT diseases Eye diseases Dental diseases Facial neuralgia and atypical facial pain: True neuralgia Trigeminal neuralgia Glossopharyngeal neuralgia Auriculotemporal neuralgia Sluder’s neuralgia Temporomandibular joint “neuralgia” (Costen syndrome) Atypical facial pain Table 12.4 Abbreviated etiologic classification of the more important causes of head- ache and facial pain, following the proposal of the Headache Classification Committee of the International Headache Society (Cephalagia 1988; 8 [Suppl. 7]: 1–96). 1. Migraine 1.1 Migraine without aura 1.2.1 Migraine with typical aura 1.2.2 Migraine with prolonged aura 1.2.3 Familial hemiplegic migraine 1.2.4 Basilar migraine 1.2.5 Migraine aura without headache 1.3 Ophthalmoplegic migraine 1.4 Retinal migraine (Cont.) General Aspects 799 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Table 12.4 (Cont.) 1.5 Childhood periodic syndromes that may be precursors to or associated with migraine 1.5.1 Benign paroxysmal vertigo of childhood 1.5.2 Alternating hemiplegia of childhood 1.6 Complications of migraine 1.7 Migrainous disorder not fulfilling above criteria 2. Tension-type headache 2.1 Episodic tension-type headache 2.2 Chronic tension-type headache 2.3Headache of the tension type not fulfilling above criteria 3. Cluster headache and chronic paroxysmal hemicrania 3.1 Cluster headache 3.1.1 Cluster headache periodicity undetermined 3.1.2 Episodic cluster headache 3.1.2 Chronic cluster headache 3.2 Chronic paroxysmal hemicrania 3.3 Cluster headache-like disorder not fulfilling above criteria 4. Miscellaneous headaches unassociated with structural lesion 4.1 Idiopathic stabbing headache 4.2 External compression headache 4.3 Cold stimulus headache 4.4 Benign cough headache 4.5 Benign exertional headache 4.6 Headacheassociatedwithsexual activity 5. Headache associated with head trauma 5.1 Acute post-traumatic headache 5.2 Chronic post-traumatic headache 6. Headache associated with vascular disorders 6.1 Acute ischemic cerebrovascular disease 6.2 Intracranial hematoma 6.3 Subarachnoid hemorrhage 6.4 Unruptured vascular malformation 6.5 Arteritis 6.6 Carotid or vertebral artery pain 6.6.1 Carotid or vertebral dissection 6.6.2 Carotidynia (idiopathic) 6.6.3 Post endarterectomy headache 6.7 Venous thrombosis 6.8 Arterial hypertension 6.9 Headache associated with other vascular disorder 7. Headache associated with non-vascular intracranial disorder 7.1 High cerebrospinal fluid pressure 7.1.1 Benign intracranial hypertension 7.1.2 High pressure hydrocephalus 7.2 Low cerebrospinal fluid pressure 7.3 Intracranial infection 7.4 Intracranial sarcoidosis and other noninfectious inflammatory diseases (Cont.) 800 12 Headache and Facial Pain Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Table 12.4 (Cont.) 7.5 Headache related to intrathecal injections 7.6 Intracranial neoplasm 7.7 Headacheassociatedwithotherintracranial disorder 8. Headache associated with substances or their withdrawal 8.1 Headache induced by acute substance use or exposure 8.2 Headacheinduced by chronic substance use or exposure 8.3 Headache from substance withdrawal (acute use) 8.4 Headache from substance withdrawal (chronic use) 8.5 Headache associated with substances but with uncertain mechanism 9. Headache associated with non-cephalic infection 10. Headache associated with metabolic disorder 10.1 Hypoxia 10.2 Hypercapnia 10.3 Mixed hypoxia and hypercapnia 10.4 Hypoglycemia 10.5 Dialysis 10.6 Headache related to other metabolic abnormality 11. Headache or facial pain associated with disorder of cranium, neck, eyes, ears, n ose, sinuses, teeth, mouth or other facial or cranial structures 11.1 Cranial bone 11.2 Neck 11.3 Eyes 11.4 Ears 11.5 Nose andsinuses 11.6 Teeth, jaws and related structures 11.7 Temporomandibular joint disease 12. Cranial neuralgias, nerve trunk pain and deafferentation pain 12.1 Persistent (in contrast to tic-like) pain of cranial nerve origin 12.1.1 Compression or distortion of cranial nerves and second or third cervical roots 12.1.2 Demyelination of cranial nerves 12.1.3 Infarction of cranial nerves 12.1.4 Inflammation of cranial nerves 12.1.5 Tolosa-Hunt syndrome 12.1.6 Neck-tonguesyndrome 12.1.7 Other causes of persistent pain of cranial nerve origin 12.2 Trigeminal neuralgia 12.2.1 Idiopathic trigeminal neuralgia 12.2.2 Symptomatic trigeminal neuralgia 12.3 Glossopharyngeal neuralgia 12.4 Nervus intermedius neuralgia 12.5 Superior laryngeal neuralgia 12.6 Occipital neuralgia 12.7 Central causes of head and facial pain other than tic douloureux 12.7.1 Anaesthesia dolorosa 12.7.2 Thalamic pain 12.8 Facial Pain not fulfilling criteria in groups 11 or 12 13. Headache not classifiable General Aspects 801 Mumenthaler, Neurology © 2004 Thieme All rights reserved. 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[...]... phe- Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license The Major Primary Headache Syndromes nomenon, but the resulting impairment in some cases depends on factors beyond the pain itself The intensity of post-traumatic headache (287b, 504a, 99 9c) seems to be inversely proportional to the severity of the precipitating trauma (777c) Migraine ( 298 a,... anorexia, weight loss, night sweats, and low-grade fever are common They are also seen in the other major form of giant-cell arteritis, namely polymyalgia rheumatica, Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license Spondylogenic Headache and Cervical Migraine which causes pain in the larger joints, particularly in the proximal segments of the... iron deficiency – e.g., in hemorrhagic anemia – can cause intractable headache Headache due to hypothyroidism has been described (674b) Morgagni-Morel syndrome, a disorder of unknown and probably heterogeneous cause affecting elderly women, consists of frontal internal hyperosto- Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license Facial Pain sis,... simultaneously or nonsimultaneously with migraine headache, accompanied by nonspecific T-wave changes on ECG The pain and the ECG changes respond to @ -blockers (575a) Migraine patients are more susceptible than other persons to acute amnestic episodes (p 387), reportedly also to coital amnesia (551a) Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license The... spreads to the whole head (1012) (p 215) There can also be persistent headache in the months and years after subarachnoid hemor- Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license 816 12 Headache and Facial Pain rhage ( 298 c) Secondary normal pressure hydrocephalus should be ruled out (p 41) Arterial Hypertension It is not known for certain whether... intracranial hypertension > Focal neurologic signs > Cranial nerve deficits Mental status, with particular attention to: > Psycho-organic syndrome > Neuropsychological deficit > Impairment of consciousness > Psychological conflicts > Depression > Neurotic personality traits Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license The Major Primary Headache... 765d, 885a) Yet it is certainly true that degenerative or post-traumatic changes of the upper three cervical segments sometimes cause transient occipital pain; they can also reactivate a pre-existing headache tendency (746a, 746b) Spondylogenic headache should be diagnosed only if the following conditions are met: Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions... in which the patient first sees a bright, colored, lightning-like figure with a zigzag border proceeding from the center to the periphery of the homonymous visual field (fortification specter) The Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license The Major Primary Headache Syndromes 8 09 Table 12.7 Treatment of acute migraine episodes (This form... are said to play an important role in so-called tension headache This not entirely unproblematic term refers to a variety of forms of headache, mostly in the occipital region, that are said to be due to shorter- or longer-lasting spasmodic contraction of the nuchal musculature, particularly at times of mental stress Tension headache is not the same thing as tension-type headache (p 803) It is not always... Habitual Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license Facial Pain bruxism (grinding of the teeth) can also lead to muscle pain in the face A selection of such conditions is listed in Table 12 .9 General Differential Diagnosis of Headache and Facial Pain A precise clinical history is essential for the correct diagnosis of pain syn- 827 dromes . pres- ence of pain in the tibial compart- ment, and the frequent but not in- variable absence of a pulse in the dor- 794 11 Lesions of Individual Peripheral Nerves Mumenthaler, Neurology © 2004 Thieme All. but the resulting impair- ment in some cases depends on fac- tors beyond the pain itself. The inten- sity of post-traumatic headache (287b, 504a, 99 9c) seems to be in- versely proportional to. pedaling movements (e.g., potters) are at risk of chronic me- chanical injury to both the tibial and the common peroneal nerves, be- Tibial Nerve 795 Mumenthaler, Neurology © 2004 Thieme All rights reserved.