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To determine the role of transcranial doppler (TCD) in the evaluation of the vertebrobasilar circulation, we compared the results of TCD with intraarterial digital subtraction angiography (DSA) in 20 patients with vertebrobasilar ischaemia (VBI). TCD had a sensitivity of 87%, a specificity of 80%, a positive predictive value of 93% and a negative predictive value of 67%. It was also able to give functional data when combined with arteriography and correctly identified the main pathology in 92% of those with abnormal TCD and angiogram. The 2 patients with false negative TCD had vertebral artery occlusion, which may be missed because of the signal from adjacent arteries. TCD may be a useful screening method in patients with VBI for the detection of large vessel occlusive disease of the intracranial vertebrobasilar system. It is important to remember that proximal vertebral artery stenoses will be missed by TCD.

Background and Purpose: We sought to determine the risks of stroke, myocardial ischemia, and vascular death in patients with asymptomatic carotid stenosis., Methods: Six hundred ninety-six patients with asymptomatic carotid stenosis referred to the Doppler laboratory were followed prospectively for a mean time of 41 months. These patients were studied both clinically and by carotid Doppler ultrasound, including evaluation of the effect of stroke risk factors., Results: Transient ischemic attacks occurred in 75 patients and stroke in 29, while 132 had ischemic cardiac events. Five patients died from stroke and 59 from cardiac causes. Annual stroke rate was 1.3% in patients with carotid stenosis less than or equal to 75% and 3.3% in those with stenosis greater than 75%. Ipsilateral stroke rate was 2.5% in patients with greater than 75% carotid stenosis. Annual cardiac event rate was 8.3% and death rate 6.5% in patients with severe carotid stenosis., Conclusions: With carotid stenosis less than or equal to 75%, the stroke rate is negligible (1.3% annually) whereas the combined risk of cardiac ischemia and vascular death is as high as 9.9%. With stenosis greater than 75%, combined transient ischemic attack and stroke rate is 10.5% per year, with 75% of events ipsilateral to the stenosed artery.

We describe 12 cases of acute stroke in which clinical features of proximal posterior cerebral artery occlusion simulated the clinical syndrome of middle cerebral artery occlusion. The majority of patients developed contralateral hemiparesis, homonymous hemianopia, hemispatial neglect, and sensory loss or sensory inattention. All 8 patients with dominant hemisphere lesions were aphasic. Accurate diagnosis in each case was achieved only after a head CT, showing occipital lobe, thalamic, and inferomesial temporal lobe infarction. "Cortical" signs are probably explained by thalamic involvement. Recognition of this syndrome has implications for management and prognosis.

Two cationic, lipophilic laser dyes, 1,1',3,3,3',3'-hexamethylindodicarbocyanine iodide (HIDC) and 1,1',3,3,3',3'-hexamethylindotricarbocyanine iodide (HITC), inhibit bovine heart mitochondrial and Paracoccus denitrificans NADH oxidase activities. The mitochondrial I50 values were 0.5 microM (HIDC) and 1.2 microM (HITC), and the P. denitrificans I50 values 1.2 microM (HIDC) and 1.5 microM (HITC). Neither succinate nor cytochrome oxidase (EC 1.9.3.1) activities were inhibited significantly by either compound, localizing the site of inhibition to the segment of each electron transport chain between NADH and ubiquinone. With submitochrondrial particles (SMP), NADH-dependent reduction of menadione, duroquinone and coenzyme Q1 was inhibited markedly (HIDC was the more potent inhibitor). Using purified complex I, only NADH-dependent reduction of duroquinone and coenzyme Q1 was inhibited markedly (HIDC was the more potent inhibitor) and reduction of menadione was inhibited slightly. With P. denitrificans membrane vesicles, NADH-dependent reduction of menadione, juglone, and coenzyme Q1 was inhibited slightly and duroquinone reduction was inhibited markedly. Membrane-dependent interactions appear to be involved, since the compounds were more inhibitory with membrane preparations than with complex I. The mechanism of inhibition (except for the HIDC effect on coenzyme Q1 reduction with P. denitrificans) appeared to be through the interaction of dye with the rotenone site on NADH-ubiquinone reductase (EC 1.6.99.3), since rotenone-insensitive preparations of complex I and P. denitrificans membrane vesicles were also insensitive to HIDC and HITC inhibition.

Using an antibody to S100 protein, the number of dendritic cells above the basal layer in the epidermis was assessed in necrobiosis lipoidica and granuloma annulare. A statistically significantly higher number of these cells was found within the epidermis in necrobiosis lipoidica compared with granuloma annulare and normal skin. The numbers were similar to those seen in sarcoidosis and tuberculous reactions in the skin, which raises the possibility of an immune pathogenesis for necrobiosis lipoidica.

The diagnosis of functional seizures is difficult and emotional factors may be important in the cause and triggering of seizures. This paper describes the evaluation to fo 15 patients with suspected functional seizures.

Suppression of the vestibulo-ocular reflex was assessed in normal subjects and patients with neurological disorders to determine the relative effects on suppression of a single fixation target and an optokinetic field. Subjects were rotated sinusoidally in yaw at varying frequencies of up to 0.5 Hz whilst seated in a Barany chair. A comparison was made between eye movements in darkness, those produced during fixation on a central target mounted to the chair, and eye movements during fixation on the target plus an "earth-fixed" or "chair-fixed" visual background. Presentation of a background produced only minimal effects on the suppression of the vestibulo-ocular reflex in normal subjects. In patients with impairment of fixation suppression, suppression of the vestibulo-ocular reflex was not improved after presentation of either form of optokinetic field. The results demonstrate that central fixation is the predominant requirement for suppression of the vestibulo-ocular reflex. This correlates closely with the ability to pursue. Although the optokinetic reflex generates following eye movements similar to pursuit, it cannot be used to mediate suppression of the vestibulo-ocular reflex in the absence of an intact pursuit system. The findings strengthen the view that the optokinetic reflex evolved to act in synergy with the vestibulo-ocular reflex in generating compensatory eye movements.

Oscillopsia during head movement occurs in patients with bilateral vestibular loss and may be transient or persistent. To investigate mechanisms underlying recovery we tested the vestibulo-ocular reflex (VOR), visual-vestibular interaction, and the cervico-ocular reflex (COR); we used a pseudorandom oscillatory stimulus with a frequency band width of 0 to 5 Hz in six patients with bilaterally absent caloric responses and in 10 normal controls. Seven control subjects had low-gain COR responses, but these were anticompensatory with respect to the VOR. Three asymptomatic patients with an absent or grossly deficient VOR had increased oculomotor responses at all frequencies when oscillated in light. Compensatory COR responses were detected in these patients but not in patients with persisting oscillopsia. In some patients with bilateral vestibular loss, augmented cervico-ocular and visual reflexes may compensate, at least partially, for an absent VOR.

The stability of the commonly used red cell radio labels chromium-51, indium-(111 or 113m), and technetium-99m, within intact red cells and stroma and their distribution within the cell were compared in undamaged and heat damaged red cells in relation to the clinical use of heat damaged cells in the assessment of splenic function. Chromium-51 labelled haemoglobin both in undamaged and heat damaged cells; indium predominantly labelled haemoglobin in undamaged cells but labelled stroma in heat damaged cells, even when the cells were labelled before heating; technetium-99m predominantly labelled haemoglobin in undamaged cells but only labelled stroma in heat damaged cells if these were heated before labelling. Indium was more firmly bound by stroma prepared from heat damaged cells, and technetium-99m showed a high rate of elution both from cells and stroma, although this rate was lower for heat damaged cells.

Four examples of patients who sustained a vestibular insult and did not fully recover over a prolonged period are described. The reasons for this failure of compensation are discussed in relation to the experimental literature, particularly that concerning the importance of extra-vestibular inputs upon the vestibular system.

Unilateral iritis, keratitis and episcleritis presented in a 45-year-old female Melanesian from New Britain, Papua New Guinea. A motile nematode was seen in the anterior vitreous but was not recovered. Inflammation resolved with topical corticosteroid and antibiotic treatment, but visual impairment persisted. She failed to return for repeat serology after discharge, and measurement of serum antibody levels to Angiostrongylus cantonensis in the single specimen obtained, using the direct and indirect immunofluorescent tests, showed a titre of 1:128. Ocular angiostrongyliasis is briefly reviewed and the differential diagnosis of intra-ocular nematode infestation is presented.

The symptom of vascular neck pain, known as carotidynia, refers to throbbing pain of the neck and face with tenderness of the carotid artery. Recent publications suggest that carotidynia is a benign complaint, frequently associated with migraine, and often responding to migraine therapy. Past experience, and our own, indicates that carotidynia may be a symptom of other more serious disorders whose identification is essential to prevent subsequent catastrophic complications. 7 patients discussed in this publication presented with carotidynia. 4 have been reported previously. The associated disorders were dissecting aneurysm of the internal carotid artery (2 patients), long intraluminal clots with incomplete vessel obstruction of the internal carotid artery (2 patients), spontaneous aneurysm of the common carotid bifurcation (2 patients) and giant cell arteritis. We conclude that carotidynia is a symptom to be regarded with suspicion. The majority of patients encountered will have 'benign' carotidynia and angiography or exploratory surgery should not be routine. A rational approach to evaluation, investigation and treatment is presented.

A case of choreoathetosis due to thalamic haemorrhage and responding to pimozide is described. The anatomical changes, the neurotransmitter abnormalities and the drug treatment of chorea are discussed.

Five hundred asymptomatic patients with cervical bruits were followed prospectively by clinical and Doppler examination for up to four years (mean, 23.2 months) to identify the variables predicting outcome. Thirty-six patients had strokes or transient ischemic attacks, 51 had cardiac ischemic events, and 45 died. At one year the incidence of cerebral ischemic events (transient ischemic attacks and strokes) was 6 percent, that of cardiac ischemic events was 7 percent, and that of death was 4 percent. The overall incidence of stroke at one year was 1.7 percent (1 percent in patients without previous transient ischemic attacks), but the incidence was 5.5 percent in patients with severe carotid-artery stenosis (greater than 75 percent). Cerebral ischemic events were most frequent in patients with severe carotid-artery stenosis (P less than 0.0001), progressing carotid-artery stenosis (P less than 0.0005), or heart disease (P less than 0.0005) and in men (P less than 0.025). The degree of carotid-artery stenosis on initial presentation was a powerful predictor of neurologic sequelae. Patients with asymptomatic cervical bruits have a higher risk of a cardiac ischemic event than of a stroke. Although the risk of cerebral ischemic events is highest in patients with severe carotid-artery stenosis, in most instances even these patients do not have strokes without some warning.

Ultrasound techniques are employed increasingly for the evaluation of patients with cerebrovascular disease. We determined the accuracy of carotid Doppler ultrasonography, which incorporated spectral analysis and periorbital directional Doppler assessment, by comparison with conventional or digital-subtraction arteriography in 93 patients (186 vessels). We also reviewed our experience with the Doppler technique in consecutive patients who were admitted to hospital with established carotid-territory stroke. The Doppler technique had a sensitivity of 93% and a specificity of 97% as a screening test for the presence of carotid stenosis, and a high level of precision. The arteriography rate in patients with completed stroke was 40% before the introduction of Doppler ultrasonography but decreased to 24% after its introduction, and to 16% in the last 100 cases. The proportion of cases in whom an underlying cause for stroke could not be identified decreased from 31% of cases to 21% of cases. Extracranial carotid stenosis was implicated in only 22 of the last 100 patients with carotid-territory stroke. Doppler ultrasonography is a valuable diagnostic tool in patients with completed stroke. It aids in the selection of patients for arteriography and provides clues to the pathogenesis of stroke in patients in whom arteriography is inappropriate.

We report a collaborative study of 11 patients with upbeat nystagmus in the primary position of gaze. In most cases the nystagmus behaved in accordance with Alexander's Law; in 3 patients convergence enhanced the nystagmus. Lateral gaze was without effect in 7 instances. Static tilt to prone and supine positions altered the characteristics of the nystagmus in 7 patients. The effects were variable and, in one case, there was reversal of the direction of the nystagmus to downbeating. There was pathological or radiological confirmation of lesions in the pontomedullary junction (2 cases) and the pontomesencephalic junction (2 cases). The findings support previous reports that primary position upbeat nystagmus occurs predominately with intra-axial brainstem lesions. There is one report of its occurrence with an intrinsic cerebellar lesion. Modification of the amplitude of upbeat nystagmus by tilt of the head with respect to gravity in the majority of patients implies an otolith-related component in the genesis of the nystagmus.

Normal pressure hydrocephalus is frequently emphasised as a cause of reversible dementia, but is seldom encountered. Over a 2 year period, 5 patients presented with cognitive decline, and gait disturbance, with or without incontinence. CT head examination revealed hydrocephalus. Although none had symptoms of raised intracranial pressure on initial presentation, there were clinical or CT signs of raised intracranial pressure in 4 of the 5. Underlying pathologies were meningeal lymphocytic lymphoma, idiopathic meningeal fibrosis, periaqueductal glioma, basilar aneurysm and basilar invagination. All patients responded to the insertion of a shunt. Over the same period, only 1 patient was shunted for idiopathic normal pressure hydrocephalus, without improvement. We challenge the concept of idiopathic normal pressure hydrocephalus as a cause of cognitive deterioration.

A patient with downbeat nystagmus and familial ataxia is described. The nystagmus was induced by static tilt away from normal upright posture, by linear acceleration of the head, and by convergence. It is inferred that the nystagmus was modulated by otolith-specific stimuli and not by stimulation of the canals. These findings demonstrate the role of otolith function in generation of eye movements in the vertical plane and support proposed interrelationships between otolith and vergence mechanisms. The nystagmus and associated oscillopsia were partially suppressed by treatment with clonazepam.

Binswanger, in his 1894 dissertation on the differential diagnosis of general paresis of the insane, described a slowly progressive dementia associated with macroscopic loss of white matter. In recent years interest in Binswanger's disease was rekindled with CT demonstration of extensive white matter low densities in some patients. To define the clinical spectrum, we reviewed 22 consecutive cases in which the CT appearances suggested a diagnosis of Binswanger's disease. Two patients had focal neurological deficits at presentation, but recent anoxic or hypoglycaemic insults could not be excluded as the cause of the CT abnormalities. The 20 remaining patients were demented and showed variable combinations of corticobulbar dysfunction and gait dyspraxia. The duration of symptoms ranged from a few months to several years. Sixty per cent of this group gave a history of discrete stroke events and focal cortical and/or lacunar infarcts were a frequent CT finding. Binswanger's disease is probably due to chronic or acute-on-chronic white matter ischaemia. The association with lacunar and cortical infarctions suggests that a combination of large and small vessel disease produces diffuse ischaemia maximal in white matter watershed zones. Binswanger's disease is clinically differentiated from multi-infarct dementia by its time course.

The performance of the smooth pursuit reflex and the ability to suppress the vestibulo-ocular reflex were assessed in 10 normal subjects and in patients with a variety of diseases of the central nervous system. Pursuit was measured as the maximum velocity of slow phase eye movement in response to a laser target moving sinusoidally at various frequencies up to 1 Hz and with amplitudes stepped up to 35° peak. Suppression of the vestibulo-ocular reflex was assessed with subjects seated in a Barany chair rotating sinusoidally in yaw at matching frequencies. The breakpoint of vestibulo-ocular reflex supression was defined as the peak velocity of oscillation at which nystagmus appeared on electro-oculographic recording as determined by the method of ascending and descending thresholds. For normal subjects, at all frequencies, the breakpoint of suppression corresponded closely with the peak velocity of pursuit at the corresponding frequency of target oscillation. In some patients pursuit and suppression were comparably impaired. In others either pursuit or suppression could be selectively impaired with the other function left intact. The results demonstrate that the mechanisms of pursuit and visual suppression of the vestibulo-ocular reflex have similar dynamics and share a common pathway at least to the level of the cerebellum. Thereafter, there is presumably an anatomical and functional dissociation of the signals mediating the two functions. The key area involved appears to be the flocculus for lesions of this structure alone cause impairment of both functions. The findings also indicate that the appropriate way to test smooth pursuit in relationship to suppression is to increase the amplitude of target oscillation until the peak slow eye movement velocity is determined for each frequency. The finding that increasing excursion increases maximum pursuit velocity supports the view that pursuit has an acceleration limit which is more critical in determining performance than velocity limitations. The results establish the assessment of vestibulo-ocular reflex suppression as a powerful test of the integrity of CNS function independent of its previous association with disordered pursuit.

The value of neck bruits as indicators of underlying carotid artery disease was assessed by correlating the results of carotid Doppler examination with auscultation in 336 patients with asymptomatic bruits. Also, the separate findings of auscultation by two physicians were compared for agreement in the quality and location of the bruits. Levels of agreement between the physicians in the clinical examination were acceptable for the presence and site of the neck bruits, but were unacceptable for the intensity, pitch, and duration. Unilateral bruits in the upper neck indicated underlying internal carotid artery (ICA) stenosis detectable by carotid Doppler (greater than 35% stenosis) in 61%, whereas only 11% of patients with bruits localized to the supraclavicular area had ICA stenosis. "Silent" contralateral ICA stenosis was detected by Doppler in 28% of patients with unilateral cervical bruits. Bilateral cervical bruits were the most powerful predictors (76%) of underlying ICA stenosis detectable by Doppler. Neck bruits are valuable indicators of underlying carotid artery disease, but Doppler ultrasound examination adds significantly to clinical accuracy.

Asymptomatic cervical bruits with their implication of underlying carotid artery disease, carry an established but low risk of stroke. In spite of the rising numbers of patients subjected to carotid endarterectomy for this condition, there is little evidence that the benefits outweight the risks. Outcome data from community studies and the current prospective Toronto study of patients with asymptomatic neck bruits indicate that the annual stroke rate is 1-2%, and the annual cardiac death rate is 2-4%. Published data of the results of carotid surgery suggest that surgical risks outweigh any possible benefits, unless a subgroup with spontaneous stroke risk of at least 5% can be identified.