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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of multiple sclerosis which began at the age of 12 years. Clinical symptoms at onset were acute, regressive cerebellovestibular ataxia and optic neuritis. Twenty-four years later vertigo, motor and sensory deficit of the right lower limb and grand mal seizures developed. CSF and MRI were suggestive of multiple sclerosis. The patient is now free of neurological symptoms with an 8 years' follow-up.
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PMID:[Benign multiple sclerosis with childhood onset]. 786 56

As dizziness can be caused by so many different pathophysiological mechanisms, it is crucial to determine the type of dizziness before proceeding with the diagnostic evaluation. Vertigo, defined as an illusion of movement, is an important subtype of dizziness that indicates a lesion somewhere within the vestibular system. Probably the most useful feature for differentiating between peripheral and central causes of vertigo is the associated symptoms. Vertigo of peripheral origin is typically associated with auditory symptoms such as hearing loss and tinnitus, while vertigo of central origin is nearly always associated with neurological symptoms such as diplopia, weakness, numbness and ataxia. Each of the common causes of vertigo has a characteristic clinical profile that should suggest a likely diagnosis after the history and examination are complete. Probably the most important treatment breakthrough is the positional manoeuvre that reliably cures benign positional vertigo (see Chapter 6). The treatment strategy for an acute peripheral vestibular lesion has evolved over the past few years. Patients are encouraged to return to normal physical activity as rapidly as possible. Repeated head, eye and body movements (vestibular rehabilitation) help the brain to recalibrate the relationship between visual, proprioceptive and vestibular signals (Chapter 9).
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PMID:Approach to the dizzy patient. 787 2

We report the clinical findings and stroke mechanisms of 63 patients with cerebellar infarcts. We divided the intracranial vertebrobasilar circulation into the proximal territory (P), fed by the intracranial vertebral arteries and their branches; the middle territory (M), fed by the proximal and middle basilar artery and its branches; and the distal territory (D), fed by the rostral basilar artery and its branches. Cerebellar infarcts were classified by vascular territories P, M, D, P&D, and middle-plus (P&M, M&D, and P&M&D). Patients with P infarcts (11 patients) frequently had vertigo, gait instability, limb ataxia, and headache, whereas patients with D infarcts (15 patients) most often had limb ataxia, gait instability, and dysarthria. Patients with P&D infarcts (17 patients) had signs and symptoms of both groups combined. Infarcts in which the middle territory was involved, either alone (three patients) or combined with other territories (17 patients) were dominated by brainstem signs and symptoms. The predominant stroke mechanisms in the P, D, and P&D groups were embolic due to intra-arterial or cardiac embolism. When the M territory was involved, either alone or with P, D, or P&D territories, stroke mechanisms were more varied, and there was often large-artery occlusion with hemodynamic ischemia.
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PMID:Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. 805 34

Twenty-two cases of cerebellar infarction were diagnosed by clinical findings, computerized tomography (CT), magnetic resonance image (MRI) and autopsy. Most of the infarctions occurred in the territory of the posterior inferior cerebellar artery (18/22). The most common and earliest symptoms were dizziness or vertigo (19/22), which occurred repeatedly and were accompanied by nausea and vomiting. The symptoms and signs of cerebellar lesion such as unsteady gait, limb and/or trunk ataxia, dysarthria were also the main clinical manifestations. However, in a number of patients there were no cerebellar symptoms or signs (9/22). Rapid deterioration of consciousness suggested acute compression of the brainstem, where the prognosis would be poor. CT scan made it possible to diagnose cerebellar infarction in the patients. But CT is not a satisfactory instrument in identifying this disease. MRI without bony artifacts from the posterior fossa has much higher resolution and renders the infarction to be visualized earlier. It may be regarded as the most ideal instrument in diagnosing this disease.
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PMID:Cerebellar infarction. Analysis of 22 cases. 808 78

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.
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PMID:Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery. 808 72

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

This report consists of 13 patients who on retrospective analysis had had periodic symptomatology in the first 2 years of life, and who on later evaluation were determined to have juvenile migraine. The commonest early expression consisted of vomiting, accompanied by behavioral change. Seven of 13 showed some indication of headache. Other symptoms such as sleep relief, pallor, and vertigo or ataxia were relatively common. A family history of migraine, primarily maternal, was found in 11 of 12 patients in whom it could be evaluated.
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PMID:Migraine in the infant and toddler. 815 Oct 93

Third ventricular ependymomas are rare tumors that have not been specifically examined. Four cases of these tumors are reported. The presenting symptoms included headache, ataxia, vertigo, and Parinaud's syndrome. All the patients underwent computed tomographic scanning and cerebral angiography, followed by craniotomy and microsurgical resection of the tumor. In addition, all patients had or developed symptomatic obstructive hydrocephalus requiring shunting procedures. Three of the patients are alive with a follow-up of 4 to 12 years. It is remarkable that these tumors are so rare, given that the ependymal surface area of the third ventricle is greater than that of the fourth. The management of these tumors should include aggressive surgical resection, radiation therapy, and cerebrospinal fluid diversion.
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PMID:Ependymomas of the third ventricle. 817 98

Vertigo related to acidosis in Meniere's disease has been reported. This study was undertaken to ascertain whether acidosis has any effect on vertigo. Since patients with Meniere's disease usually show unilateral vestibular dysfunction, unilateral intratympanic injection of streptomycin sulfate (SM) was used to induce unilateral vestibular dysfunction in rabbits. Intratympanic SM injections induced vestibular destruction and elicited severe spontaneous nystagmus and ataxia. Then symptoms of acute vestibular upset gradually subsided and eventually disappeared completely. Three weeks after SM injections, in compensated rabbits, NH4Cl injection or CO2 inhalation was used to induce acidosis. Intravenous NH4Cl injection or CO2 inhalation induced nystagmus and ataxia again. In normal rabbits, no nystagmus was induced by NH4Cl injection or by CO2 inhalation. These results suggest that acidosis might be a cause of recurrence of vertigo in patients with unilateral vestibular dysfunction.
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PMID:Effect of experimental acidosis on nystagmus in rabbits. 820 92

Infarction of the cerebellum comprises about 1.5 percent of all strokes. The symptoms are initially very similar to those of benign labyrinthitis, and the diagnosis is easy to miss. There are three major causes of clinical deterioration and death: Expansion of the infarct to the brainstem, swelling of the infarcted cerebellum with compression of the brainstem, and hydrocephalus. Surgical intervention may be lifesaving if hydrocephalus develops. Five patients admitted to our department are described. All described sudden vertigo or dizziness, which in three of them was accompanied by headache. All had ataxia. In four this was ipsilateral to the infarction and in one bilateral. Two had slight hemiparesis and plantar inversion. Two patients developed hydrocephalus. One was operated with external drainage. It is important to have this diagnosis in mind in all patients with acute labyrinthine symptoms. Acute CT scanning should be carried out if the patient becomes less conscious.
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PMID:[Cerebellar infarctions]. 823 75


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