After unilateral cerebral hemisphere stroke, resulting in contralateral arm symptoms but largely sparing higher cerebral function, ipsilateral arm function is generally considered to be unaffected. In this study, 8 subjects with acute unilateral cerebral infarction (confirmed by CT scan) and primarily motor deficits underwent 11 computerized and 6 clinical assessments between 11 days and 12 months poststroke, and were compared with 12 normal subjects. Computerized tests comprised 3 pursuit tracking tasks (preview-random, step and a combination of these), designed to measure different aspects of integrated sensory-motor (S-M) function, and 12 tasks aimed at breaking tracking into various sensory, perceptual and motor components (joint movement sense, visual resolution, object perception, static and dynamic visuospatial perception, range of movement, grip and arm strength, reaction time, speed, static and dynamic steadiness). The asymptomatic arm was impaired on all but one of the computerized tests throughout the 12-month period, although to a lesser degree than the symptomatic arm. Grip strength was marginally impaired initially. Incomplete neurological recovery was seen in the asymptomatic arm for all functions except strength, speed and steadiness, possibly indicating their resistance to improvement. Clinical assessment detected no asymptomatic arm impairment and only a mild transient deficit of higher mental function. Our data suggest that (1) all cerebral hemisphere areas involved in S-M functions can exert some degree of bilateral motor control; (2) ipsilateral influence is never greater than contralateral influence, and is usually considerably less; and (3) the proportion of ipsilateral to contralateral control is closely related to the degree of continuous sensory feedback required by the particular task. The mechanism and degree of ipsilateral dysfunction can be explained by a 3-tier cerebral model of S-M integration comprising a lower level of functions with high contralateral specificity (somatosensory and motor), a middle level of non-limb-specific partially lateralized functions (ideomotor praxis and visuospatial perception) and an upper level of global mental activities (intellect, alertness, etc.).

No abstract

Chronic progressive hepatocerebral degeneration with spastic paraparesis, dementia, dysarthria, ataxia, tremor, and neuropsychiatric symptoms follows long-standing portal-systemic shunting, is associated with structural changes in the central nervous system, and does not respond to conventional therapy for hepatic encephalopathy. A case of advanced chronic liver disease with severe, progressive hepatocerebral degeneration after 23 yr of portal-systemic shunting is reported in whom there was significant objective improvement in intellectual function and in the chronic neurological signs 3 mo after orthotopic liver transplantation and further improvement 12 mo after transplantation.

Background-Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis. Case Description-We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. Serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, Ͻ3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low-and high-frequency domains (0.04 and 0.06 ms 2 , respectively; normal level, 0.14Ϯ0.02 ms 2 ). MNSA was increased in frequency (61 bursts per minute; normal level, 34Ϯ18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact. Key Words: baroreflex Ⅲ hypertension Ⅲ lateral medullary syndrome Ⅲ stroke N eurogenic hypertension has been demonstrated in animal models and is well known to occur in humans after subarachnoid hemorrhage, hydrocephalus, and stroke. 1 Blood pressure (BP) is increased after stroke, particularly after lacunar infarction or hemorrhage and in patients with preceding hypertension. 2,3 It is usually maximal on day 1 and may fall more during the first week in those with higher initial values. 4 The mechanism may involve a transient increase in sympathetic activity or baroreflex dysfunction, although current evidence for this is unsatisfactory. Spectral analysis techniques, measuring heart rate (HR) and BP variability, suggest that baroreflex sensitivity is decreased after a cortical stroke. 5 Serum catecholamine levels are raised in some patients during the first week. 6 In addition to being increased, BP may also become more variable after stroke. 7 Paroxysmal neurogenic hypertension has been associated with a variety of pathologies affecting the brain stem but has only rarely been attributed to stroke. 1 We describe a case of paroxysmal hypertension after left lateral medullary infarction and demonstrate, using microneurographic recordings of sympathetic activity, that the likely mechanism was partial baroreflex failure. Conclusions-Extensive Case ReportA 75-year-old woman presented with sudden onset of slurred speech, double vision, and left-sided incoordination. She was on long-term treatment for essential hypertension consisting of cyclopenthiazide 0.5 mg daily and nadolol 40 mg BID. Examination findings were consistent with a left-sided lateral medullary syndrome and included the following: rotatory nystagmus on left gaze; left-sided Horner's syndrome, facial hemiane...

Two patients presenting with dysphagia due to cricopharyngeal muscle dysfunction developed limb weakness 2 to 3 years later. Cricopharyngeal and limb muscle biopsies demonstrated changes typical of inclusion body myositis (IBM). Both patients improved following cricopharyngeal myotomy. IBM should be considered in patients presenting with dysphagia.

The aim of this study was to determine the performance of a PC-based system for real-time detection and topographical mapping of epileptiform activity (EA) in the EEG during routine clinical recordings. The system incorporates a mimetic stage to locate candidate spikes (including sharp-waves) followed by two expert-system-based stages, which utilize spatial and wide-temporal contextual information in deciding whether candidate events are epileptiform or not. The data comprised 521 consecutive routine clinical EEG recordings (173 hours). Performance was evaluated by comparison with three independent electroencephalographers (EEGers-I). A second group of two EEGers (EEGers-II) separately interpreted the spike topographical maps and, for EEGs categorized as containing only questionable EA by the detection system, reviewed 6 sec segments of raw EEG centered on each questionable event. Thirty-eight of the EEGs were considered to contain definite EA by at least two of EEGers-I. The false detection rate of the system was 0.41 per hour. The system was found to have a sensitivity of 76% and a selectivity of 41% for EEGs containing definite EA. However, it only missed detection of EA in 5% of the recordings. EEGers-II agreed with EEGers-I on the distribution (generalized, lateralized, focal, multifocal) of EA in 79% of cases. This is by far the largest clinical evaluation of computerized spike detection reported in the literature and the only one to apply this in routine clinical recordings. The false detection rate is the lowest ever reported, suggesting that this multi-stage rule-based system is a powerful and practical tool in clinical electroencephalography and long-term EEG monitoring.

SUMMARY Excitability changes following a nerve impulse were studied in the rat tail. Supernormal nerve excitability in control animals was present, as in other vertebrate nerve fibres, from 4-30 ms and was followed by a period of subnormal excitability extending up to Narahashi and Anderson,3 and Narahashi4 used the giant axons of the cockroach and later of the squid and crayfish to show that allethrin, one of the earliest synthetic pyrethroids to be developed, induced changes of this kind which were associated with a prolonged negative after potential. At high dosage the action potential gradually decreased in amplitude until conduction block occurred. Using a voltage clamp technique the latter authors correlated these findings with a prolongation in the inward sodium current across the membrane and decrease in the steady state outward potassium current. Similar findings have been described at single nodes of Ranvier following the application of allethrin and more recently of a newer potent synthetic pyrethroid, deltamethrin, previously called decamethrin.56 The deltamethrin-induced prolongation of the sodium current appears, however, to be of much longer duration (over one second) than that induced by allethrin (up to one hundred milliseconds).5 The long inward sodium current is believed to be due to the prolongation of membrane permeability to sodium resulting from sodium channels which, having opened upon depolarisation, remain open for longer than normal. The effects of pyrethroids on sodium channel kinetics have been the subject of recent study.6 7 In normal nerve fibres the sequence of changes in excitability that follow an action potential induced by a single stimulus are now well established and are regarded as a general feature of axonal physiology.8 Although much of this evidence is 337

Abstract-It is critically important for certain occupational groups to remain highly alert throughout their working day. For safety reasons, it would be useful to automatically detect lapses in performance using EEG/EOG. Automating the detection process could be simplified considerably if we could mimic human experts. Surprisingly, it is unclear to what extent human EEG raters are able to detect lapses. Consequently, we undertook a study in which 4 expert EEG raters assessed the level of alertness of 10 air traffic controllers by observing a combination of their EEG and EOG while they performed a 10 min psychomotor vigilance task (PVT). They were specifically required to identify lapses or sleep episodes that might lead to a lapse in PVT performance. A reaction time 500 ms was defined as a PVT lapse. There was a total of 101 lapses (mean duration = 1.00 s). Of these, only 6 lapses were detected by one or more raters and all of these were marked as 'sleep'. Overall the human expert raters were unable to reliably identify lapses based only on EEG and EOG. This poor performance suggests an automated system would need to identify subtle features not overtly visible in the EEG.