Postmortem examination of relapsing acute Guillain-Barre syndrome.
We report a patient who had six episodes of acute Guillain-Barre syndrome during his life. He is the fifth such case with postmortem analysis.
Biomedical subjects
Publications and source records attributed to R B Daroff.
We report a patient who had six episodes of acute Guillain-Barre syndrome during his life. He is the fifth such case with postmortem analysis.
A 29-year-old woman presented with acute hemicrania, trigeminal neuropathy and posterior fossa dysfunction. The admission differential diagnosis included vertebral artery dissection, posterior circulation aneurysm, vascular malformation and brainstem infarction. However, radiographic and CSF studies indicated demyelination. Acute demyelination should be in the differential diagnosis of vascular hemicrania with signs of posterior fossa dysfunction.
Since headache is one of the most common symptoms experienced in the general population, the neuroscience nurse should understand the phenomenon of migraine. We define the various types of migraine and present a strategy, based upon precipitators, inhibitors and a "migraine threshold" to facilitate patient education.
Latent/manifest latent nystagmus (LMLN) is a jerk nystagmus with a decreasing-velocity or linear slow phase whose fast phase is in the direction of the fixating eye. Change of the fixating eye by alternating tropias or cover will cause reversal of the LMLN to preserve this relationship. In the dark, where no fixation is possible, the fast phases of LMLN are in the direction of the intended fixating eye; actual visual input will override this effect of intention. A patient with persistent hyperplastic primary vitreous of the right eye, which was enucleated at age 9 due to glaucoma, had LMLN with fast phases to the left. His congenitally blind right eye was replaced with an ocular prosthesis whose movements were conjugate with his seeing eye. In the dark, we found that his LMLN spontaneously reversed as the normally fixating left eye became esotropic. Furthermore, as is the case with LMLN patients who have sight in both eyes, he was able to willfully reverse his LMLN in the dark by alternating his "fixating" eye. We conclude from these observations that the direction of LMLN is determined at a cortical level, is intimately related to the intended fixating eye and that eye "dominance" is predetermined and not altered by visual abnormalities, including blindness.
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The general notion that space motion sickness (SMS) is due to a "conflict" between vestibular, visual, and other sensory inputs has gained popular acceptance. We have reviewed three specific hypotheses for SMS and identified characteristic disorders of ocular motility that each hypothesis would predict. Accurate recording of horizontal and vertical eye movements during free head movements in space craft presents technical difficulties. We suggest that careful clinical examination may be useful, provided the examination is directed towards detecting those specific abnormalities predicted by each hypothesis.
Accurate ocular motility recordings were made of the saccadic responses of five patients with Eaton-Lambert syndrome (ELS). It was found that, contrary to common belief, the ocular motor system is affected. The saccades of ELS patients mimicked those of patients with myasthenia gravis (MG). Both groups exhibited hypometria and multiple, closely spaced saccades. Two patients demonstrated both saccadic facilitation and positive edrophonium tests. The ELS patients had slow or normal saccadic velocities, not the "super-fast" velocities found in patients with ocular MG.
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A 65-year-old man with ischaemic encephalomalacia following surgery for an aortic arch aneurysm experienced episodes of stereotyped formed visual hallucinations uniquely provoked by television viewing. In addition he noted vertical diplopia of cerebral origin. These symptoms are discussed in the light of what is known about visual hallucinations, television-induced epilepsy, and cerebral polyopia.
A clinical constellation of aseptic meningitis, arachnoiditis, communicating hydrocephalus, and a Guillain-Barré syndrome occurred following lumbar myelography with metrizamide. To our knowledge, Guillain-Barré syndrome has not been previously described following myelography with any contrast agent. Meningeal reactions and hydrocephalus have been reported with other agents, but this is the first instance with metrizamide.
We treated 67 patients with the symptoms of benign paroxysmal positional vertigo (BPPV) by challenging them with the precipitating head positions on a repeated and serial basis. Sixty-six of the patients experienced complete relief of the vertigo within three to 14 days; in two patients, the vertigo recurred but responded to a second course of therapy. The one patient whose condition did not respond was found to have a perilymphatic fistula that mimicked BPPV. The presumed mechanism for this therapy is the loosening and ultimate dispersion of degenerated otolithic particles from the cupula of the posterior semicircular canal.
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