Biomedical subjects
Publications and source records attributed to B T Troost.
We present a common cause of vertigo, benign positional paroxysmal vertigo (BPPV), and its history, diagnosis, and therapy. BPPV is suggested by history, readily diagnosed by office examination, and cured by appropriate exercise therapy. Since the condition is so common and often unrecognized, physicians are encouraged to consider BPPV as a possible cause of treatable dizziness.
BACKGROUND: Earlier reports of cocaine-associated cerebral vasculitis have been based primarily on angiographic findings without pathological verification. CASE DESCRIPTION: We present a case of acute encephalopathy following intravenous and intranasal administration of cocaine. Brain biopsy revealed vascular changes involving primarily small arteries. Findings included lymphocytic infiltration, endothelial thickening, and deposition of proteinaceous amorphous material within and around vessel walls. CONCLUSIONS: These abnormalities are consistent with pathological features of arteritis previously reported in association with amphetamine and multiple-drug abuse. Vasospasm-induced changes are an alternative explanation for the vascular picture seen in this case. The patient made modest improvement with high-dose intravenous steroids.
Amaurosis fugax in a younger person in whom premature atherosclerotic disease and cardiac emboli have been eliminated is usually benign. We describe a 25-year-old man with recurrent painless left monocular visual loss lasting from 5 to 45 minutes. Initial physical examination, carotid ultrasound, and electrocardiogram were normal. Goldmann visual field testing demonstrated a small, left paracentral defect. Neuroimaging studies were initially declined for economic reasons, but later a magnetic resonance image disclosed a large pituitary tumor displacing the left optic nerve and chiasm. The tumor was removed via a transphenoidal approach, and the episodic visual symptoms disappeared. We stress that amaurosis fugax in young patients is not necessarily benign. A specific etiology should be diligently sought, particularly when ocular signs are present.
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We describe a patient with papilledema due to benign intracranial hypertension who had sudden, painless monocular visual loss. Fear of further visual deterioration prompted vigorous therapeutic efforts to reduce intracranial pressure. Subsequent neuro-ophthalmologic evaluation disclosed that the visual loss was due to a subretinal neovascular membrane. Vision continued to improve after medical therapy was discontinued, and was accompanied by complete resolution of papilledema and headache. In any patient with minimal papilledema, sudden visual deterioration should initiate a search for other causes rather than zealous therapeutic efforts to reduce intracranial pressure.
A patient had a thirteen-year history of symptoms clinically indistinguishable from classic migraine: a slowly progressive visual fortification spectrum lasting 40 minutes, followed by a five- to six-hour throbbing unilateral headache with nausea and vomiting. After unsuccessful migraine therapy, investigation revealed a large occipital lobe arteriovenous malformation (AVM). Surgical removal of the AVM resulted in immediate and total resolution of all symptoms.
A 52-year-old steelworker displayed a consistent defect in leftward voluntary gaze across the midline. Both fast (saccadic) and slow (pursuit) eye movements were affected. Neuro-ophthalmologic evaluation revealed no additional neurologic or ophthalmologic deficit. Pupilary miosis occurred during leftward gaze attempt, indicating that the gaze palsy was due to spasm of the near reflex. Special maneuvers during clinical eye movement testing disclosed full ability to make normal horizontal fast and slow eye movements despite the apparent defect in "voluntary" leftward gaze.
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The results of quantitative infrared horizontal eye movement recordings in 8 patients with progressive supranuclear palsy are presented. Some of the patients had total paralysis of vertical movements, but none had completely lost the ability to perform horizontal eye movements. All patients had a defect in ocular fixation previously undescribed in this condition: the universal presence of square-wave jerks. Analysis of refixation saccades demonstrated hypometria, slow velocity/amplitude relationships, and profound prolongation of duration. The pursuit abnormality, characterized clinically by "cogwheel" eye movements, represented the inability to match eye velocity to target velocity. The ratio of peak eye velocity to peak target velocity (pursuit gain) was 0.2 to 0.5. Defects in the vestibuloocular reflex included inability to increase the gain of the reflex (ratio of peak eye velocity to head velocity) during viewing of a visible, stationary target and failure to suppress the reflex when viewing a target rotating with the head.
We observed a 69 year old patient who had spontaneous paroxysmal attacks of weeping with lacrimation, contorted facies, and (usually) head-turning to the right. These episodes were followed by confusion and amnesia. During a pentylenetetrazol-evoked attack the EEG showed a right temporal delta rhythm. Atrophy, particularly of the right temporal regions, was noted on pneumoencephalography. We propose the term "dacrystic epilepsy" for this rare type of seizure disorder.
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The differentiation of migraine headache, preceded by visual aura, from cerebral arteriovenous malformation (AVM) is often regarded as difficult. A study of 26 patients with occipital lobe AVM revealed two distinct syndromes in 18 patients--occipital epilepsy and occipital apoplexy. Occipital epilepsy is characterized either by elementary visual phenomena, such as brief flashes of light, or by dimming of a homonymous field. Occipital apoplexy results from hemorrhage and hematoma formation within the occipital lobe and is characterized by sudden headache and homonymous visual field loss. We conclude that patients harboring occipital AVMs may, indeed, have visual phenomena and headache that should not be confused with migraine because either a history of generalized seizure or bruits on examination will probably be present.
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Tuberous sclerosis and Klippel-Trenaunay-Weber (KTW) syndromes are phakomatoses which are believed to be inherited separately. A 41 year old woman presented with the classic features of tuberous sclerosis: adenoma sebaceum, mental retardation, and seizures. In addition, the diagnostic triad of KTW involved the left lower limb: cutaneous naevi, a vascular anomaly, and osteohypertrophy. Arteriography documented the presence of visceral tumours and an arteriovenous malformation of the leg. This is the first reported association of the fully-developed symptomatology of tuberous sclerosis and KTW in one person.
Quantitative eye movement recordings in a patient with multiple sclerosis who had both macro square wave jerks and an internuclear ophthalmoparesis supported the concept of an internal brain-stem monitor that mediates corrective eye movements. A brain-stem model of this monitor illustrates the patient's motility disorder and the normal function of providing synergistic version and vergence corrections for dysmetric eye movements. Thus, the careful study of pathologic disturbances provides information relevant to the normal operation of the ocular motor system.
The peak velocity-amplitude characteristics of voluntary saccades and the fast phases of caloric, rotational, and optokinetic (OKN) nystagmus were compared in ten human subjects in both light and, except for OKN, darkness. All these fast eye movements had similar velocities and all slowed in darkness. This study supports the presumption that the identical brainstem firing patterns found in monkeys for all fast eye movements also occur in man.