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PubMed1978

Double-blind trial of oral papaverine in chronic cerebrovascular ischemia.

A preliminary analysis of the effect of long-term therapy with oral papaverine has been made in 11 patients with chronic cerebral ischemia due to cerebral arteriosclerosis. The cases were classified as remote cerebral infarction (6 patients) or vertebrobasilar arterial insufficiency (5 patients). The patients received 225 mg or 450 mg daily, assigned in a double-blind manner. Most showed clinical improvement and improvement on the EEG. There was a statistically significant increase in regional cerebral blood flow in the vertebrobasilar arterial distribution, including the brain stem and cerebellar and posterior cerebral regions, particularly in the right hemisphere. Evidence appears to indicate that zones of severe remote cerebral infarction are refractory to pharmacologically induced vasodilation.

Administration, Oral↗
PubMed1975

Ocular skew deviation. Analysis of 100 cases.

In 100 patients with ocular skew deviation, the lesion was usually on the side of the lower eye, particularly when patients with internuclear ophthalmoplegia were excluded, but exceptions were sufficiently frequent to diminish the clinical lateralizing value of skew. Pontine damage was most commonly encountered, but midbrain-pretectal and medullary lesions were frequent. The onset of skew frequently coincided with acute brain stem damage, and while a wide variety of diseases produced skew deviation, stem strokes were present in more than two thirds of the patients. The hypothesis that skew results from damage to tonic otolith-ocular pathways is generally compatible with both the known anatomy of otolith pathways and the clinical presentation of skew. Otolith function testing in patients with skew, further anatomical definition of otolith-ocular pathways, and clinicopathological study of discrete lesions associated with skew should help resolve the causative role of the otolith organs in skew deviation.

Adolescent↗
PubMed1993

Pharyngeal constrictor paresis: an indicator of neurologic disease?

Pharyngeal constrictor paresis (PHCP) is sometimes found in videoradiography of the swallowing act in patients complaining of dysphagia. Ten patients with PHCP and 10 dysphagic, age- and sex-matched controls with normal videoradiography were neurologically evaluated and examined with magnetic resonance imaging (MRI) of the brain and brainstem in order to learn the pathogenetic process behind PHCP. The study revealed 8 PHCP patients and 1 dysphagic control with abnormal clinical neurological findings such as myopathy, cerebrovascular disease, or extrapyramidal disease. The neurological examination revealed considerable information of prognostic and therapeutic value in PHCP patients. The MRI was abnormal in 7 PHCP patients and 4 dysphagic controls. However, the findings in MRI were nonspecific but the examination was found to be valuable in selected cases. It is concluded that PHCP is an indicator of neurological disease and accordingly, such patients should be examined by a neurologist to establish the cause of the disease.

Adult↗
PubMed1996

Laser-evoked cerebral potentials and sensory function in patients with central pain.

Central pain syndromes (CPS) could be caused by disinhibition of spinothalamic excitability or by other central nervous system (CNS) changes caused by reduced spinothalamic function. To examine these possibilities, we studied 11 patients (ages 51-82 years) with unilateral central pain and with reproducible cerebral evoked vertex potentials in response to cutaneous stimulation of the normal side with pulses from an infra-red CO2 laser. All patients had normal tactile and kinesthetic sensation; one had slightly decreased vibratory sense bilaterally. All showed, from the unaffected (asymptomatic) side, laser evoked potentials (LEPs) with negative (N) components ranging from 208 to 280 msec peak latency (av: 240 +/- 6 SE msec) and peak amplitudes of 1-7 microV (av: 2.9 +/- 0.5 SE microV), followed, in all but 1 patient, by positive (P) potentials ranging from 288 to 370 msec peak latency (av: 319 +/- 7.7 SE msec) with peak amplitudes of 1-7 microV (2.8 +/- 0.5 SE microV). Laser stimulation of the affected (symptomatic) side in 5 patients evoked LEPs with N-P interpeak amplitudes that were within 20% of those evoked from the normal side. All but one of these patients had thresholds for warm, heat pain, and deep pain that were normal in comparison with the unaffected side. The excepted patient had the largest N-P interpeak amplitude asymmetry (18.5%) of this group. Ratings of laser pulse intensity were either symmetrical (n = 2) or increased on the affected side (n = 3) in these patients. In contrast, laser stimulation of the affected side failed to evoke either N or P potentials in 6 patients, all of whom had lateralized increased thresholds for warm, heat pain, or deep pain, or reduced ratings of laser pulse sensation. Although 1 patient had increased ratings of laser pulse sensation, the amplitude of the LEP was always reduced on the side of increased pain or heat threshold in these CPS patients (Fisher exact test: P = 0.015). These results reflect primarily a deficit in spinothalamic tract function and do not suggest excessive CNS responses to synchronous activation of cutaneous heat nociceptors in patients with CPS.

Aged↗
PubMed1992

Stroke and dolichoectatic intracranial arteries.

During a 6-year-period, in 45 patients the diagnosis of dolichoectatic intracranial arteries was established. Dolichoectasia of the vertebrobasilar system was the most frequent finding (n = 39). Twenty-two patients presented with brain stem ischaemia, and 10 patients had ischaemic hemispheric events. Six patients had symptoms due to compression of cranial nerves. Hydrocephalus was observed once. Peak and mean flow velocities in 39 patients with dolichoectatic basilar arteries as revealed by transcranial Doppler ultrasound were significantly reduced (p less than 0.00001) when compared with an age-adjusted control group of 20 patients without evidence of vertebrobasilar dolichoectasia on angiogram. Non-invasive MR-angiography offered an excellent imaging of the vascular abnormality. The combined use of CT, TCD, MRI and MR-angiography allows reliable non-invasive diagnosis of dolichoectatic intracranial arteries. This condition seems to play an underestimated role in stroke patients, in particular with respect to the vertebrobasilar circulation.

Brain Ischemia↗
PubMed1982

Acquired pendular nystagmus: its characteristics, localising value and pathophysiology.

Investigations were made of 16 patients with acquired pendular nystagmus and a further 32 cases reported in the literature were reviewed. Amongst our own patients two thirds had multiple sclerosis, almost one third a cerebrovascular accident or angioma and two had optic atrophy with squint. The nystagmus took forms which could be monocular or binocular, conjugate or disconjugate and could involve movements about single or multiple axes. Spectral analysis was used to characterise the amplitude and frequency of the movements and to estimate the degree of relationship (coherence) between movements of the two eyes or between movements of one eye about several axes. The oscillations ranged in frequency from 2·5 Hz to 6 Hz, with typical amplitudes between 3° and 5°. In a given patient all oscillations, regardless of plane, were highly synchronised. Somatic tremors of the upper limb, face and palate associated with the nystagmus were often at similar frequencies to the eye movement. The other ocular signs common to all our patients were the presence of squint with failure of convergence. Most patients also had skew deviation or internuclear ophthalmoplegia or both. The major oculomotor systems, that is, saccades, pursuit, optokinetic and vestibulo-ocular reflexes could be intact. It is inferred that the mechanism responsible for the pendular nystagmus lies at a level which is close to the oculomotor nuclei so that it can have monocular effects but is not part of the primary motor pathways. It is possible that this mechanism normally subserves maintenance of conjugate movement and posture of the eyes. The periodicity of the nystagmus is likely to arise from instability in a certain type(s) of neurone, for the associated somatic tremors have similar characteristics and yet involve very different neuronal muscular circuitry. Prognosis for cessation of the nystagmus is poor. In five patients with multiple sclerosis it was suppressed by intravenous hyoscine with, however, unacceptable subsequent side effects.

Adult↗
PubMed2002

Sudden deafness and anterior inferior cerebellar artery infarction.

BACKGROUND AND PURPOSE: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be associated with vertigo, nystagmus, facial weakness, and gait ataxia. Few reports have carefully examined the deafness associated with the AICA infarction. Furthermore, previous neurological reports have not emphasized the inner ear as a localization of sudden deafness. The aim of this study was to investigate the incidence of deafness associated with the AICA infarction and the sites predominantly involved in deafness. METHODS: Over 2 years, we prospectively identified 12 consecutive patients with unilateral AICA infarction diagnosed by brain MRI. Pure-tone audiogram, speech discrimination testing, stapedial reflex testing, and auditory brainstem response were performed to localize the site of lesion in the auditory pathways. Electronystagmography was also performed to evaluate the function of the vestibular system. RESULTS: The most common affected site on brain MRI was the middle cerebellar peduncle (n=11). Four patients had vertigo and/or acute auditory symptoms such as hearing loss or tinnitus as an isolated manifestation from 1 day to 2 months before infarction. Audiological testings confirmed sensorineural hearing loss in 11 patients (92%), predominantly cochlear in 6 patients, retrocochlear in 1 patient, and combined on the affected side cochlear and retrocochlear in 4 patients. Electronystagmography demonstrated no response to caloric stimulation in 10 patients (83%). CONCLUSIONS: In our series, sudden deafness was an important sign for the diagnosis of AICA infarction. Audiological examinations suggest that sudden deafness in AICA infarction is usually due to dysfunction of the cochlea resulting from ischemia to the inner ear.

Adult↗
PubMed1995

When is isolated vertigo a harbinger of stroke?

Isolated vertigo is usually a distressing though benign clinical entity. Recently, however, it has been recognized that in a subset of patients isolated vertigo may be a harbinger of vertebrobasilar stroke. Recognition of this "at risk" subgroup may be difficult. Brainstem auditory evoked potentials (BAEPs) are usually normal in patients with vertigo from labyrinthine disease. We describe a patient with isolated vertigo, in whom BAEPs were abnormal, and who subsequently developed an anterior inferior cerebellar artery territory infarct. BAEP testing might lead to early recognition of those patients at risk for catastrophic stroke, and prompt appropriate investigation and treatment to prevent this outcome.

Cerebral Infarction↗
PubMed1984

[Obstructive hydrocephalus in cerebellar infarcts].

Large cerebellar ischaemic infarction may act as a space-occupying lesion and cause acute ventricular dilatation secondary to brain stem compression. 8 cases are regarded and the clinical course and therapy are discussed. After acute onset with vestibular and cerebellar symptoms, signs of progressive clouding of consciousness, accompanied often by signs of brain stem compression develop leading finally to decerebration syndrome. CT reveals an extensive hypodense area, usually in the lower part of the cerebellar hemisphere, compression and shift of the IVth ventricle and dilatation of 3rd and lateral ventricles. Drainage of ventricular fluid alone is not sufficient and the therapy of choice is the resection of infarcted tissue. Even in patients, who were operated in the early phase of decerebration excellent recovery was noted.

Adult↗
PubMed1994

Neurovascular complications of cocaine.

Use of cocaine in the USA, has reached epidemic proportions since 1983, when "crack" was introduced, its higher potency compared with cocaine HCl has been associated with a tremendous increase in the incidence of strokes. This study reports our experience with 55 cases of neurovascular events (25 ischemic and 30 hemorrhagic) related to cocaine use in 54 patients. Only 15 patients had other risk factors for stroke. Twenty six patients smoked "crack", 10 snorted cocaine and 12 injected it intravenously. Strokes occurred within 3 h of cocaine use in 15 patients with infarcts and 17 with hemorrhages. Ten infarcts occurred after an overnight binge. Of the hemorrhage group 9 were subarachnoid, 16 intracerebral (8 basal ganglia, 7 hemispheric and one brain stem) and 5 intraventricular. Computerized tomography (CT) showed an aneurysm of the anterior communicating artery, as well as one of the vein of Galen. Four aneurysms and 3 AVMs were identified on angiography. CT revealed 15 infarcts; it was normal in 7 patients with pure motor hemiparesis and in 3 with findings consistent with anterior spinal artery infarction. Several mechanisms may be responsible for the cerebrovascular complications. A sudden rise in systemic arterial pressure may cause hemorrhages, frequently in association with an underlying aneurysm or AVM. Vasospasm, arteritis, myocardial infarction with cardiac arrhythmias and increased platelet aggregation may provoke infarcts.

Adult↗
PubMed1996

Contralateral cerebellar hemorrhagic infarction after pterional craniotomy: report of five cases and review of the literature.

OBJECTIVE AND IMPORTANCE: Five cases of cerebellar hemorrhagic infarction complicating pterional craniotomy are presented. Recognition of this rare complication may be delayed, with catastrophic consequences, because clinicians are unaware of the possibility. We suggest that the mechanism of this complication is dislocation of the dependent part of the cerebellum and venous obstruction causing hemorrhagic infarction. CLINICAL PRESENTATION: Five patients undergoing pterional craniotomies for benign conditions (four unruptured aneurysms and one meningioma) developed hemorrhagic infarction of the contralateral cerebellum in the postoperative period. This resulted in obstructive hydrocephalus and brain stem compression. A review of the literature revealed only one previous report of a similar complication in patients with gross coagulopathy. This was not a problem in our patients. INTERVENTION: The time of onset of symptoms varied from immediately postoperative to 24 hours later. Once the diagnosis was made, the hydrocephalus was drained and the posterior fossa was decompressed. CONCLUSION: The outcome depended on two variables: 1) the rate of development of hemorrhagic infarction and the associated complications and 2) the amount of time that elapsed before remedial action was taken. Two patients with the first signs of deterioration in the immediate postoperative period had the worst outcome; one died and the other remained severely disabled. In two patients with good neurological recovery, problems were identified and corrected within 4 hours of the first sign of deterioration. Rapid overdrainage of cerebrospinal fluid during supratentorial surgery should be avoided, and the fluid volume should be replaced before closure. Postoperative evaluation of patients whose conditions deteriorate after supratentorial craniotomy should include adequate imaging studies of the posterior fossa.

Cerebellar Diseases↗