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CEREBROVASCULAR DISEASES
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Figure 34-13 (Continued)
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Signs and symptoms 1 Medial medullary syndrome (occlusion of vertebral artery or branch of vertebral or lower basilar artery) a On side of lesion (1) Paralysis with later hemiatrophy of the tongue b On side opposite lesion (1) Paralysis of arm and leg sparing face (2) Impaired tactile and proprioceptive sense over half the body 2 Lateral medullary syndrome (occlusion of any of ve vessels may be responsible vertebral, posterior inferior cerebellar, or superior, middle, or inferior lateral medullary arteries) a On side of lesion (1) Pain, numbness, impaired sensation over half the face (2) Ataxia of limbs, falling to side of lesion (3) Vertigo, nausea, vomiting (4) Nystagmus, diplopia, oscillopsia (5) Horner syndrome (miosis, ptosis, decreased sweating) (6) Dysphagia, hoarseness, paralysis of vocal cord, diminished gag re ex (7) Loss of taste (rare) (8) Numbness of ipsilateral arm, trunk, or leg (9) Hiccup b On side opposite lesion (1) Impaired pain and thermal sense over half the body, sometimes face 3 Total unilateral medullary syndrome (occlusion of vertebral artery); combination of medial and lateral syndromes 4 Lateral pontomedullary syndrome (occlusion of vertebral artery); combination of medial and lateral syndromes 5 Basilar artery syndrome (the syndrome of the lone vertebral artery is equivalent); a combination of the various brainstem syndromes plus those arising in the posterior cerebral artery distribution The clinical picture comprises bilateral long-tract signs (sensory and motor) with cerebellar and cranial nerve abnormalities a Paralysis or weakness of all extremities, plus all bulbar musculature b Diplopia, paralysis of conjugate lateral and/or vertical gaze, internuclear ophthalmoplegia, horizontal and/or vertical nystagmus c Blindness, impaired vision, various visual eld defects d Bilateral cerebellar ataxia e Coma f Sensation may be strikingly intact in the presence of almost total paralysis Sensory loss may be syringomyelic or the reverse or involve all modalities
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Issuing twelfth nerve Pyramidal tract Medial lemniscus
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Descending tract and nucleus of fth nerve Uncertain restiform body, cerebellar hemisphere, olivocerebellar bers, spinocerebellar tract ( ) Vestibular nuclei and connections Vestibular nuclei and connections Descending sympathetic tract Issuing bers ninth and tenth nerves Nucleus and tractus solitarius Cuneate and gracile nuclei Uncertain Spinothalamic tract
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Corticobulbar and corticospinal tracts bilaterally Ocular motor nerves, apparatus for conjugate gaze, medial longitudinal fasciculus, vestibular apparatus Visual cortex Cerebellar peduncles and the cerebellar hemispheres Tegmentum of midbrain, thalami Medial lemniscus, spinothalamic tracts or thalamic nuclei
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sis, ptosis, decreased sweating); issuing bers of the ninth and tenth nerves (hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, diminished gag re ex); otolithic nucleus (vertical diplopia and illusion of tilting of vision); olivocerebellar and/or spinocerebellar bers and restiform body and inferior cerebellum (ipsilateral ataxia of limbs, falling or toppling to the ipsilateral side, or lateropulsion); descending tract and nucleus of the fth nerve
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(pain, burning, and impaired sensation over ipsilateral half of the face); nucleus and tractus solitarius (loss of taste); and rarely cuneate and gracile nuclei (numbness of ipsilateral limbs) Fragmentary syndromes are more frequent at the onset of the stroke; the fragmentary syndromes are vertigo and ptosis, toppling and vertical diplopia, hoarseness and disequilibrium, etc Vertigo alone, however, is not an indication of lateral medullary infarction The small-
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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
est infarction we have studied gave rise only to symptoms of lateropulsion and mild ipsilateral limb ataxia The eye signs of lateral medullary infarction may be dif cult to interpret Often there is a fragment of an internuclear ophthalmoplegia or a skew deviation (the globe on the affected side usually higher) Direction changing nystagmus (with different head positions) is said to be the most useful feature that distinguishes labyrinthine disease from brainstem forms of nystagmus, but infarction of the vestibular nucleus as part of the lateral medullary syndrome may also show this sign (see also Chap 15) The entire lateral medullary syndrome, one of the most striking in neurology, is almost always due to infarction, with only a small number of cases being the result of hemorrhage or tumor Although it was traditionally attributed to occlusion in the course of the posterior inferior cerebellar artery (PICA), careful studies have shown that in 8 out of 10 cases it is the vertebral artery that is occluded by atherothrombosis; in the remainder, either the posterior inferior cerebellar artery or one of the lateral medullary arteries is occluded Embolism is a less frequent cause The inferior cerebellum is usually affected, causing vomiting, vertigo, and ataxia In recent years, we have become aware from our own patients that although most of those with lateral medullary infarction do well and have considerable recovery, sudden and unexpected death may occur from respiratory or cardiac arrest, sometimes even in the absence of cerebellar swelling or basilar artery thrombosis Cases of this nature have been reviewed by Norving and Cronqvist The related and important issue of cerebellar swelling after vertebral artery or PICA occlusion and the subsequent need for surgery is discussed under Treatment of Cerebral Edema and Raised Intracranial Pressure, later in the chapter Basilar Artery The branches of the basilar artery may be instructively grouped as follows: (1) paramedian, 7 to 10 in number, supplying a wedge of pons on either side of the midline; (2) short circumferential, 5 to 7 in number, supplying the lateral two-thirds of the pons and the middle and superior cerebellar peduncles; (3) long circumferential, 2 on each side (the superior and anterior inferior cerebellar arteries), which run laterally around the pons to reach the cerebellar hemispheres (Figs 34-11 and 34-12); and (4) several paramedian (interpeduncular) branches at the bifurcation of the basilar artery and origins of the posterior cerebral arteries supplying the high midbrain and medial subthalamic regions These interpeduncular and other short proximal branches of the posterior cerebral artery have been described above The picture of basilar artery occlusion due to thrombosis may arise in several ways: (1) occlusion of the basilar artery itself, usually in the lower or middle third at the site of an atherosclerotic plaque and superimposed thrombosis; (2) occlusion of both vertebral arteries; and (3) occlusion of a single vertebral artery when it is the only one of adequate size Also, thrombosis may involve a branch of the basilar artery rather than the trunk (basilar branch occlusion) When there is embolism, the clot usually lodges at the upper bifurcation of the basilar or in one of the posterior cerebral arteries, since the embolus, if it is small enough to pass through the vertebral artery, easily traverses the length of the basilar artery, which is of greater diameter than either vertebral artery The syndrome of basilar artery occlusion, as delineated by Kubik and Adams, re ects the involvement of a large number of structures: corticospinal and corticobulbar tracts, cerebellum, middle and superior cerebellar peduncles, medial and lateral lemnisci, spinothalamic
tracts, medial longitudinal fasciculi, pontine nuclei, vestibular and cochlear nuclei, descending hypothalamospinal sympathetic bers, and the third through eighth cranial nerves (the nuclei and their segments within the brainstem) The complete basilar syndrome comprises bilateral long tract signs (sensory and motor) with variable cerebellar, cranial nerve, and other segmental abnormalities of the brainstem Often the patient is comatose because of ischemia of the high midbrain reticular activating system Others are mute and quadriplegic but conscious, re ecting interruption of descending motor pathways in the base of the pons but sparing of the reticular activating system ( lockedin syndrome; see page 305) Midbasilar disease may also cause coma if the posterior communicating arteries are inadequate to perfuse the distal basilar artery territory In the presence of the full syndrome, it is usually not dif cult to make the correct diagnosis The aim should be, however, to recognize basilar insuf ciency long before the stage of total de cit has been reached The early manifestations (in the form of TIAs) occur in many combinations, described in detail further on (page 692) Basilar Branch Occlusion Occlusion of branches at the bifurcation (top) of the basilar artery results in a remarkable number of complex syndromes that include, in various combinations, somnolence or coma, memory defects, akinetic mutism, visual hallucinations, ptosis, disorders of ocular movement (convergence spasm, paralysis of vertical gaze, retraction nystagmus, pseudoabducens palsy, retraction of upper eyelids, skew deviation of the eyes), an agitated confusional state, and visual defects These have been reviewed by Petit and coworkers and Castaigne and associates as paramedian thalamic, subthalamic, and midbrain infarction syndromes and by Caplan as the top of the basilar syndrome The main signs of occlusion of the superior cerebellar artery are ipsilateral cerebellar ataxia of the limbs (middle and/or superior cerebellar peduncles); nausea and vomiting; slurred speech; and loss of pain and thermal sensation over the opposite side of the body (spinothalamic tract) Partial deafness, static tremor of the ipsilateral upper extremity, an ipsilateral Horner syndrome, and palatal myoclonus have also been reported, but we have not seen these With occlusion of the anteroinferior cerebellar artery (AICA), the extent of the infarct is extremely variable, since the size of this artery and the territory it supplies vary inversely with the size and territory of supply of the posteroinferior cerebellar artery (PICA) The principal ndings are vertigo, vomiting, nystagmus, tinnitus and sometimes unilateral deafness; facial weakness; ipsilateral cerebellar ataxia (inferior or middle cerebellar peduncle); an ipsilateral Horner syndrome and paresis of conjugate lateral gaze; and contralateral loss of pain and temperature sense of the arm, trunk, and leg (lateral spinothalamic tract) The tinnitus may be overwhelming, called screaming by some of our patients If the occlusion is close to the origin of the artery, the corticospinal bers may also be involved, producing a hemiplegia; if distal, there may be cochlear and labyrinthine infarction Cerebellar swelling has not occurred in our cases or in the 20 collected by Amarenco and Hauw The most characteristic manifestation of all these branch or division brainstem infarcts is the crossed cranial nerve and long tract sensory or motor de cit These crossed syndromes, which may involve cranial nerves III through XII, are listed in Table 34-3 Although the nding of bilateral neurologic signs strongly suggests brainstem involvement, it must be emphasized that in many instances of infarction within the basilar territory, the signs are lim-
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