Cases reported "Atrophy"

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1/5. Non-MS recurrent demyelinating diseases.

    The introduction of MRI has shown that the acute, recurrent (R), and multiphasic (M) forms of disseminated encephalomyelitis (DEM) are more common than suspected in adults, and that their MR images are sufficiently characteristic in most instances to make differentiation from multiple sclerosis (MS) possible. In addition, a number of clinical features of DEM are rarely seen in MS: fever, malaise, nausea, vomiting, positional vertigo, convulsions, aphasia, meningism, bilateral optic neuritis, and CSF leukocytosis and elevated protein. CSF oligoclonal bands are usually absent. It is remarkable that confusion between R- and MDEM and MS persists despite the numerous published reports on recurrent DEM dating back 70 years, many illustrating the characteristic MRIs. There are many case reports of DEM erroneously diagnosed as MS, Schilder's, Marburg's, Devic's, and Balo's disease, and, in particular brain tumors. It is probable that acute DEM is occasionally mistaken for a clinically isolated symptom of MS. Possible mechanisms for recurrence include localization at the site of a previous injury to the nervous system, or by the phenomenon of molecular mimicry. The importance of differentiating R- and MDEM from MS is greater today due to the recommendation that immunodulatory treatment be initiated in patients with a clinically isolated syndrome, or when the occurrence of a second clinical episode establishes the diagnosis of MS.
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ranking = 1
keywords = vertigo
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2/5. Delayed endolymphatic hydrops and its relationship to Meniere's disease.

    Delayed endolymphatic hydrops (EH) can be characterized as having ipsilateral and contralateral types. They are similar in that both have early and late phases of otologic symptoms and that the early phase is a profound hearing loss in one ear. The late phases differ, however, in that the ipsilateral type develops the symptoms of EH (episodic vertigo) in the deaf ear and the contralateral type develops the symptoms of EH (fluctuating hearing loss and/or episodic vertigo) in the hearing ear. In more than half the cases of both types of delayed EH, the profound hearing losses in the early phase are simply discovered to be present in early childhood without a known time of onset. The temporal bones of two patients with contralateral delayed EH show pathologic changes in the deaf ears that are similar to those known to occur in mumps and measles labyrinthitis, whereas the pathologic changes in the hearing ears are similar to those known to occur in Meniere's disease. These observations support the proposition that Meniere's disease may occur as a delayed sequela of inner ear damage sustained during an attack of subclinical viral labyrinthitis occurring in childhood.
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ranking = 2
keywords = vertigo
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3/5. Pathophysiology of positional vertigo of the malignant paroxysmal type.

    It is well known that paroxysmal positional vertigo is induced by change of head position and subsides immediately when the head is returned to the original position. There are two types of paroxysmal positional vertigo. One is what DIX and HALLPIKE (1952) call the benign type which is thought to be caused by otolith lesions. Another is a malignant type, in contrast to the former and is related to a lesion in the central nervous system. Otologists are usually familiar with the former, but the latter is not known among neurologists and neurosurgeons. We experienced 37 cases of the malignant type and found that this type of paroxysmal vertigo is induced by various diseases. Furthermore, we believe that the mechanism of this paroxysmal vertigo is the lack of inhibitory function of the vestibular cerebellum, and not abrupt malfunction of communication of the cerebrospinal fluid in the ventricular system. We also believe that this symptom is a very useful sign for diagnosing lesions of the cerebellar vermis.
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ranking = 8
keywords = vertigo
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4/5. Repetitive paroxysmal nystagmus and vertigo.

    A 55-year-old woman had paroxysms of vertigo and visual blurring associated with complex combined torsional, horizontal, and vertical nystagmus. These episodes occurred regularly at 2-minute intervals, each attack lasting for 15 seconds. Between attacks, there was a much finer asymptomatic nystagmus whose components were in the opposite direction to those associated with the paroxysmal attacks. A brain MRI revealed an arteriovenous malformation in close proximity to the left vestibular nucleus, with evidence of previous bleeding. Caloric testing demonstrated a left-sided vestibular paresis. We suggest that neurons in this patient's damaged left vestibular nucleus are usually underactive but regularly produce pathologic brief bursts of hyperactivity causing episodic reversal and gross exacerbation of her resting nystagmus. Treatment with low-dose carbamazepine was successful in abolishing both the paroxysms of nystagmus and the symptoms of vertigo and visual disturbance.
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ranking = 6
keywords = vertigo
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5/5. Bilateral distal upper limb amyotrophy and watershed infarcts from vertebral dissection.

    BACKGROUND: Vertebral artery disease may give rise to lower motor neuron deficits, but the pathogenesis is unknown. I describe a man with a right vertebral artery dissection who developed bilateral distal upper extremity amyotrophy. He had symmetrical bilateral focal hyperintensites of the anterior cervical spinal cord on magnetic resonance imaging, compatible with watershed infarction. CASE DESCRIPTION: A 39-year-old man developed sudden vertigo, chest and bilateral arm pain, bilateral arm weakness, and wasting involving muscles innervated by the sixth cervical to the first thoracic spinal cord segments. magnetic resonance imaging showed an extensive right vertebral artery dissection and a right posterior inferior cerebellar infarct. Magnetic resonance scans showed a small focal hyperintensity in the region of each anterior horn, extending from the mid to lower cervical spinal cord. Minimal recovery of function was present after 3 months. CONCLUSIONS: Unilateral vertebral artery dissection may give rise to disabling bilateral upper extremity amyotrophy. Watershed infarction within the anterior spinal artery territory, involving both anterior horns, appears to be the mechanism of the lower motor neuron injury.
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ranking = 1
keywords = vertigo
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