Showing papers in "Brain in 1986"

Frontal lobe dysfunction in Parkinson's disease. The cortical focus of neostriatal outflow.

Abstract: This study investigates the hypothesis that, as a consequence of Parkinson's disease, disturbed caudate outflow will lead to deficits in cognitive functions dependent upon the integrity of the prefrontal cortex, the cortical focus of caudatofugal signals. Since Parkinson's disease also involves lesions in extra-striatal midbrain cells which reduce the extrinsic supply of dopamine to this cortical region, such functions are at double risk. Forty nondemented parkinsonian patients were drawn from a pool of 100 consecutive patients and matched with 40 normal control subjects according to age, education, IQ, and sex. All patients were quantitatively rated on neurological indices of disease. Neuropsychological assessment of the patient and normal groups included tests of general intelligence, psychomotor skills, memory, visuospatial and executive functions. No global cognitive decline was observed in the parkinsonian group. Moreover, memory and visuospatial abilities were generally intact. A small cluster of deficits emerged, interpreted as reflecting impairment in the ability to spontaneously generate efficient strategies when relying on self-directed task-specific planning. In addition, several tests thought to be sensitive to frontal lobe function distinguished patients with symptoms strongly lateralized to the right versus left side of the body. Deficits in strategic planning were later investigated in relation to severity of disease and to patient attributes including IQ and age, both of which were relevant to performance on specific tasks. Results were compared with previous investigations in parkinsonian patients and discussed from the perspective of both animal and human studies involving damage to the cerebral cortex and basal ganglia. As the prefrontal cortex is thought to play a crucial role in self-directed behavioural planning, the validity of an outflow model in predicting the consequences of caudate nucleus dysfunction was supported.

An acute axonal form of Guillain-Barré polyneuropathy.

Abstract: Five patients with a clinical diagnosis of acute Guillain-Barre polyneuropathy (GBP) had electrically inexcitable motor nerves. All were quadriplegic. One patient died and 3 of the 4 survivors showed poor recovery. Autopsy studies on the patient who died showed severe axonal degeneration in nerve roots and distal nerves without inflammation or demyelination. Electrophysiological studies in these patients suggested that the predominant process was axonal degeneration. These cases may represent a separate clinicopathological entity, and constitute a variant of GBP characterized by an acute axonal neuropathy.

The contributions of motor cortex, nigrostriatal dopamine and caudate-putamen to skilled forelimb use in the rat.

Abstract: Skilled forelimb use was studied in rats with unilateral lesions of the sensorimotor cortex, the caudate-putamen, or the dopaminergic nigrostriatal bundle, in a task involving reaching for food. Limb preference and efficiency were evaluated, as well as the relationship between limb use, spontaneous, and methamphetamine-induced rotation bias, both preoperatively and postoperatively. To induce use of the nonpreferred limb, a bracelet, which prevented reaching but not other movements, was attached to the forearm of the preferred forelimb. Whereas small cortical lesions of the forepaw area of the sensorimotor cortex mildly influenced limb preference and use, larger lesions changed preference. Furthermore, medium-sized sensorimotor cortex lesions impaired contralateral limb use, although surprising recovery occurred on the forced tests with the bracelet. Large cortical lesions abolished effective reaching even on the forced tests. Impairments similar to those following sensorimotor cortex lesions were also obtained following small and large caudate-putamen lesions. By contrast, unilateral dopamine depletions not only blocked use of the limb contralateral to the depletion but also impaired use of the ipsilateral limb. There was recovery in use of the ipsilateral forelimb but not the contralateral forelimb. Correlational analysis showed a weak relation between methamphetamine-induced rotation and limb preference preoperatively but no significant relation between these two variables postoperatively. The similarity in the deficits following sensorimotor cortex lesions and basal ganglia lesions suggests that skilled forelimb use depends upon a shared neural organization within the two systems.

The clinical features of mitochondrial myopathy.

Abstract: The clinical features of 66 patients with histologically defined mitochondrial myopathy are described. The age of onset of symptoms ranged from birth to 68 years, but was before 20 years in 61%. Nineteen patients had similarly affected relatives. Three groups of cases could be identified clinically: a combination of progressive external ophthalmoplegia and weakness of the limbs induced or increased by exertion (55%); such limb weakness alone (18%); and those with clinical features, such as ataxia, dementia, deafness, involuntary movements and seizures, predominantly or exclusively arising from the CNS (27%). There was considerable overlap between these groups, and pigmentary retinopathy, present in 36% of patients, occurred in all three. At a mean disease duration of twenty years, 9 patients (all from Group 3) were severely disabled but 42 were still able to work. In vitro studies of mitochondrial metabolism, performed in 33 cases, most commonly showed deficiencies of the mitochondrial respiratory chain localized to complex I (18 patients) or complex III (9). No typical clinical picture emerged for any of the identifiable biochemical defects.

Performance of simultaneous movements in patients with Parkinson's disease.

Abstract: Ten right-handed patients with Parkinson's disease and 9 normal subjects performed five different types of movements as rapidly as possible in their own time: isotonic elbow flexion through an angle of 15 deg ('flex'); isometric squeezing of a force transducer between thumb and fingers ('squeeze'); isotonic finger flexion ('cut'); simultaneous performance of both 'flex' and 'squeeze'; simultaneous performance of 'flex' and 'cut'. The patients performed the separate movements of 'flex', 'squeeze' and 'cut' more slowly than normals. However, a more striking deficit was seen when a 'flex' and a 'squeeze' had to be performed at the same time, and with the same arm. There was an additional increase in movement times over and above that seen in the separate movements alone. If the patients used both arms ('flex' with the right, 'squeeze' with the left), rather than one, or when a 'flex' and a 'cut' had to be combined in the same arm, only a slight increase in movement times was observed. In normals, however, the speed of individual movements of 'flex', 'squeeze' or 'cut' was the same irrespective of whether they were performed separately or simultaneously. In any one subject, movement times for the separate components of 'flex' and 'squeeze' varied independently during the performance of the simultaneous movement. Because they remain independent, we suggest that when 'flex' and 'squeeze' are performed at the same time, two separate motor programmes are superimposed to produce the combined movement. In Parkinson's disease there may be a deficit in superimposing two separate motor programmes which leads to the pronounced slowness of simultaneous movements with the same arm. Comparison of movement times for a 'flex' (but not for a 'squeeze') in the separate and simultaneous movements showed that the degree of clinical akinesia was more closely related to the additional slowness in simultaneous movements than to the slowness seen when the movements were performed separately. The degree of disturbance in superimposing separate motor programmes may determine the amount of clinical akinesia in patients with Parkinson's disease.

Crossed cerebellar diaschisis. Further studies.

Abstract: To investigate further the topographical, clinical and temporal correlates of crossed cerebellar diaschisis (CCD) after supratentorial stroke, 55 patients suffering from a single unilateral ischaemic stroke in the carotid artery territory were studied with the quantitative oxygen-15 steady-state technique and positron tomography. Fourteen patients had one or more follow-up studies, contributing a total of 72 studies. The phenomenon of CCD, defined by depressed oxygen consumption in the contralateral cerebellum, was statistically significant in 58% of the studies. It was more prominent when the supratentorial infarct involved the internal capsule or the cortical mantle extensively, consistent with the hypothesis that it results from destruction of the corticopontocerebellar fibres. Although CCD was associated with the presence of hemiparesis, it also occurred in patients without hemiparesis and was not seen in all those with hemiparesis, suggesting that destruction of the pyramidal tract is neither necessary nor sufficient to induce CCD. Finally, CCD tended to persist over long periods of time after a stroke, pointing towards a transneuronal degeneration possibly akin to crossed cerebellar atrophy as a likely explanation for CCD. Nevertheless, CCD could be seen within hours of a stroke and sometimes disappeared within a few days, suggesting a temporal continuum between early, potentially reversible functional hypometabolism (diaschisis) and irreversible degeneration.

Effects of thalamic stroke on energy metabolism of the cerebral cortex. A positron tomography study in man.

Abstract: Positron emission tomography was used to study the effects of unilateral vascular thalamic lesions on cortical oxygen and glucose utilization in 10 patients. There was significant ipsilateral cortex hypometabolism in 9 of the 10 patients, affecting the whole cortical mantle diffusely. The only patient spared was free of neuropsychological deficit at the time of positron emission tomography. In 4 patients, the magnitude of ipsilateral cortical hypometabolism was significantly less at a follow-up PET study, when neuropsychological function had improved. When taken together, the 14 studies showed a significant tendency for the hypometabolism to improve with time after clinical onset. These data suggest that the ipsilateral cortical hypometabolism results from damage to the thalamocortical connections and reflect either loss of nonspecific activating afferences or a degenerative deafferentation-deafferentation process, or both. Its links with the concept of diaschisis are suggested by its tendency to recover. A causal relationship between cortical hypometabolism and neuropsychological deficit, however, although strongly suggested, cannot be firmly established from the present data.

Poststroke depression and lesion location. An attempted replication.

Abstract: Recent evidence suggests that poststroke depression is associated with the location of the brain infarct, proximity to the frontal pole being associated with greater depression following left hemisphere injury, and an opposite relationship being seen with injury to the right hemisphere. This study was designed to replicate and extend previous investigation of this issue. Depression was assessed following recent stroke in patients with localized right (n = 16) or left (n = 19) hemisphere lesions. No overall differences between these groups were found on several measures of depression. Although there appeared to be a negative linear relationship between severity of depression and distance of the lesion from the frontal pole in left hemisphere patients, this association failed to attain statistical significance. A curvilinear relationship was evident in right hemisphere patients, with anterior and posterior lesions associated with high depression scores. These data support the notion that lesion location is associated with the severity of poststroke depression, although the nature of this association may be more complex than has previously been suggested.

Electrophysiological differences between subtypes of dementia.

Abstract: The distinction between subtypes of dementia, in particular between 'cortical' and 'subcortical' dementias, is controversial. In order to study this we recorded the long latency auditory evoked potential in demented patients with clinically definite Huntington's disease, Parkinson's disease, and Alzheimer's disease. We compared the peak latencies of the components of this response both between these groups and with normal subjects, controlling for the effects of age. We found highly significant electrophysiological differences not only between the subcortical group (combined patients with Huntington's and Parkinson's disease) and the cortical group (patients with Alzheimer's disease), but also within the subcortical group itself. Using the pattern of electrophysiological response alone, we were able to classify correctly most of our patients using a logistic regression model. These results support the notion that there are distinguishable subtypes of dementia.

Structural brain correlates of emotional disorder in multiple sclerosis.

Abstract: SUMMARY Eighty-seven patients with definite multiple sclerosis (MS) were examined neurologically and administered the Mini-mental State examination (MMS) to asses cognitive disability at the beginning and end of a one-year study. A CT scan was performed in 37. A group of 16 patients with stable spinal cord injuries (SCI) were studied in a similar manner. Of the MS patients, 47% had a mean General Health Questionnaire (GHQ) score in the abnormal range. This was a higher rate than in SCI patients (p = 0.004). Mean depression scores were similar in MS and SCI patients, but MS patients with brain involvement were more depressed than those with cord lesions only (p = 0.05). Depression score was unrelated to functional disability but was correlated with the degree of neurological impairment (p = 0.03). Euphoric patients were more likely to have brain involvement (P = 0.006), to have progressive MS (P < 0.0001), and to have enlarged ventricles (P = 0.04) and were more impaired cognitively (P = 0.04) than noneuphoric patients. These results suggest that depression in MS patients is partly determined by the presence of brain involvement, but that it is also an emotional reaction to the disorder Euphoria and cognitive disorder are reflections of brain involvement.

Visuospatial function in parkinson's disease

Abstract: SUMMARY Previous research on visuospatial function in Parkinson's disease is reviewed The present experiment was designed to test two fundamental aspects of spatial ability, namely right-left discrimination and the manipulation of those concepts in different spatial perspectives Measures of accuracy and reaction time were taken The performance of patients with Parkinson's disease did not differ from that of normal subjects in the spatial components of the task. Neither a review of the literature, nor the results of the present study, give support to the idea of a generalized visuospatial deficit in Parkinson's disease.

Movement preparation in Parkinson's disease. The use of advance information.

Abstract: The effects of advance information on movement planning in parkinsonism were assessed by means of movement precuing. Using this technique, the response latencies of identical sets of movements were compared across conditions in which the degree and type of advance movement information were manipulated. Specifically, prior information concerning three movement dimensions (the direction and extent of forthcoming movements, as well as the limb to be used) was or was not provided. Eight patients with Parkinson's disease and 8 neurologically normal age-matched controls served as subjects The experiment showed that the elevated reaction times of the parkinsonian subjects are not primarily caused by delays in response selection. Estimates of specification times for each of the three dimensions showed only a modest slowing in parkinsonians. The specification of those movement dimensions unknown before the response signal appears to occur serially, and can occur in a variable order as in normals. Since parkinsonians can initiate movements with shorter latencies when partial or complete information is available, albeit more slowly than normals, we conclude that response selection and specification processes preceding rapid discrete movements are relatively unaffected by the disease. The overall slowness in movement initiation in parkinsonians as compared with normals may in part be caused by excessive delays in motor time and, in general, to those ‘input’ and/or ‘output’ processes which are unaffected by advance information.

Autosomal recessive distal muscular dystrophy as a new type of progressive muscular dystrophy. Seventeen cases in eight families including an autopsied case

Abstract: A new type of progressive muscular dystrophy, autosomal recessive distal muscular dystrophy, is described, based on observations on 17 cases (8 males and 9 females) in 8 families, including an autopsied case. The disease developed in young adults. Muscle weakness and atrophy were most marked in the distal parts of the legs, especially in the gastrocnemius and soleus muscles, and then spread to the thighs and gluteal muscles. Early impairment of standing on tip-toe with retention of the ability to stand on the heels was conspicuous. Difficulty in climbing stairs, standing up and walking subsequently appeared, but rarely progressed to confinement to bed. The forearms became mildly atrophic, with decrease in grip strength, but the small hand muscles were spared. The EMG showed myopathic changes and nerve conduction was normal. Serum creatine kinase activity was characteristically increased up to 100-fold in the early stages of the disease. It was also markedly increased in subjects in the preclinical stage and mildly in some heterozygotes. Muscle biopsies revealed myopathic changes with severe segmental necrosis accompanied by regeneration. The changes were similar to those of Duchenne muscular dystrophy. An autopsied case, aged 68 years, showed generalized muscle abnormalities with a distal predominance. The muscles in the lower legs, especially those of the calves, were severely affected. No lesions were found in the brain, spinal cord or peripheral nerves.

The effects of lateralized frontal lesions on mood regulation

Abstract: A group of Vietnam veterans with penetrating brain wounds to the orbitofrontal, dorsofrontal, and nonfrontal cortex were compared with a stratified control group on self-report and observed measures of mood state and cognition. In particular, hypotheses regarding the regulation of anxiety by frontal cortical mechanisms were evaluated. Results indicated that patients with right orbitofrontal lesions were prone to abnormally increased ‘edginess’/anxiety and depression, whereas patients with left dorsofrontal lesions were prone to abnormally increased anger/hostility. A working model of mood state regulation is presented which represents the thesis that mood sensations are subject to numerous cognitive and biological influences that result in a variety of expressions of a particular mood disorder.

Face recognition and lipreading. A neurological dissociation.

Abstract: Two cases with medial occipitotemporal ischaemic infarction in the territory of the posterior cerebral artery are discussed, neither was aphasic. The patient with the right -sided lesion is prosopagnosic and topographagnosic and is impaired at recognizing or classifying facial expressive gestures but can lipread speech efficiently. The other patient, with only a left -sided lesion, shows no deficits in face recognition nor in the classification of faces in terms of nonverbal messages, but is alexic and impaired at lipreading. It is argued that processing faces for verbal information (lipreading) and processing faces for nonverbal information (face recognition and interpretation of emotive and gestural messages) are functionally dissociated in the human brain. Theoretical interpretations of prosopagnosia that stress a perceptual component to all types of face recognition failure may therefore be misleading, for similar stimulus processing mechanisms are likely to be required to identify a speech sound from a face as to identify a nonverbal gesture of the mouth. Only the associative properties of the task differ.

Sensory effects in man of lesions of the posterior columns and of some other afferent pathways

Abstract: Clinical observations are presented on the sensory effects of lesions of different afferent pathways of the spinal cord, correlated whenever possible with histological evidence of the location and extent of the lesions. They are based on personal cases and on significant cases in the literature, including posterior column section, other causes of damage to the posterior columns, and cases of commissural myelotomy. It is concluded that the traditional view of the effects of lesions of the posterior columns is correct, but that evidence from cases proved by postmortem examination is still needed. When the information normally supplied by the posterior columns is cut off, primary sensibility for light touch and pressure is not lost, but any kind of discrimination is disturbed. There is also a disturbance in knowledge of movement and position, ataxia, and clumsiness in the use of the hands. These defects greatly affect the palpatory examination of objects and, although they may appear slight on routine neurological examination, they can cause severe disturbances in the activities of daily living. For tactile modalities, a lesion of the spinothalamic complex causes minimal or no defects and a lesion of the posterior columns causes only slight defects, whereas a lesion of both pathways gives rise to total loss of tactile and pressure sensibility in the part of the body served by both pathways. This conclusion is based on 2 cases with combined commissural myelotomy and anterolateral cordotomy. The following disturbances of mechanoreception attributed to lesions of the posterior columns are discussed: lability of threshold, persistence of sensation, tactile and postural hallucinations and temporal and spatial disturbances. In man, lesions of the posterior columns cause an increase in pain, tickle, warmth and cold. Cases are presented with and without lesions of the posterolateral columns in conjunction with lesions of one or both anterolateral columns. As these lesions did not affect sensation and as there was no difference in the sensory state following anterolateral cordotomies with or without involvement of the posterolateral column, it is concluded that lesions of this column have no effect on sensation. Cases with lesions of the anterior two-thirds of the cord are also presented to illustrate the sensory state with only the posterior third of the cord intact. In these cases, tactile and pressure sensibility and knowledge of movement and position are normal.

Sympathetic activity in man after spinal cord injury

Abstract: SUMMARY Microelectrode recordings were made in peroneal muscle nerve fascicles in 9 patients with traumatic spinal cord lesions at the C5 to T8 level. In 4 patients the lesion was incomplete with some sensibility but no voluntary motor function below the level of the lesion. All patients had increased tendon jerks. EMG was recorded in 5 patients and showed signs of some peripheral denervation. Simultaneous recordings from nerves to skin and to muscle were made in 2 patients and control recordings were made in 19 normal subjects In the patients, spontaneous neural activity was sparse but after a latency of 0.5–1 Is strong mechanical and electrical stimuli applied to the skin below the level of the lesion, stimulation of the urinary bladder and deep breaths induced bursts of efferent impulses with a conduction velocity of 0.65 m.s-1. The discharges were often followed by cutaneous vasoconstriction and/or reduction of skin resistance. It is concluded that the neural bursts contained sympathetic impulses of spinal origin. The main differences between patients and normal subjects were (1) spontaneous muscle sympathetic activity was much lower in the patients; (2) no evidence of arterial baroreflex modulation of muscle sympathetic activity was obtained in the patients; and (3) in the patients a given stimulus induced sympathetic reflex discharges which occurred synchronously in muscle and skin nerve branches. Increases of intravesical pressure induced only weak increases of muscle sympathetic activity in the patients but nevertheless marked hypertensive reactions occurred. It is suggested that the excitability of decentralized spinal sympathetic neurons to muscles is usually decreased and that mechanisms other than exaggerated sympathetic outflow must be important for evoking episodes of high blood pressure in patients with spinal cord injuries.

Proprioception with the proximal interphalangeal joint of the index finger: Evidence for a movement sense without a static-position sense

Abstract: Proprioceptive ability with the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the index finger in human subjects was examined using a method that could assess static-position sense independently of movement sense (Clark et al., 1985). The similarity in location and function of these joints would suggest similar proprioceptive mechanisms, but proprioceptive ability was found to be quite different for the two joints. The method of distinguishing a static-position sense from a movement sense was based on whether a subject's ability to detect a small change in joint position was impaired when the rate of rotation was progressively reduced. An awareness of static-position should not depend on the rate at which a joint is placed into position. However, if subjects use movement signals to detect changes in joint position, slowing the rate of displacement should reduce the intensity of these signals and make the displacements more difficult to detect. This method indicated a static-position sense with the MCP joint but only a movement sense with the PIP joint. It was confirmed that sensory input from regions of skin not stretched or deformed by rotation of the joint can influence proprioceptive sensibility with the fingers. Anaesthesia of the tip of the index finger or of the thumb blunted subject's perceptions of movement of the PIP joint of the index finger. However, anaesthesia of the PIP joint itself had no observable effect on the ability to sense movement of the joint.

Parkinson's disease and depression

Abstract: The possibility of an ‘organically’ based depression intrinsic to the pathophysiology of Parkinson's disease (PD) and comparable to endogenous depression (Major Depressive Episode) has been raised. It has also been argued that signs of depression observed in PD are merely the natural reaction of the patients to their progressive and inevitable physical limitations and loss of independent function Because conventional depression rating scales are limited in scope, a psychometric investigation of depression in PD was pursued Based on the known impairment of short-term memory (STM) in endogenous depression, which was confirmed in a group of psychiatric patients in the present study, measures of STM were also obtained in groups of depressed and nondepressed PD patients and in 15 normal control subjects. Regardless of depression severity, PD patients performed as well as control subjects and both these groups consistently obtained scores significantly better than those of the endogenously depressed patients A relative weakness in the PD patients on order-dependent STM tests was further explored and interpreted as an indication of mild frontal lobe dysfunction It was concluded that PD patients are frequently depressed when confronted with their behavioural limitations and that this reaction may be exacerbated by a form of emotional lability related to pathophysiological processes which may involve prefrontal cortical areas.

Audiogenic startle reflex of man and its relationship to startle syndromes. A review.

Abstract: The normal human audiogenic startle reflex is defined from a review of the literature, substantiated by a current investigation of normal subjects, and clarified pathophysiologically by a discussion of animal experimentation. The basic information is used to evaluate critically a variety of syndromes loosely termed 'startle' in the past. A new classification of startle syndromes is proposed.

Cortical hypoperfusion as a possible cause of 'subcortical aphasia'.

Abstract: The study was designed to investigate whether aphasia in stroke patients with subcortical lesions (‘subcortical aphasia’) was due to the subcortical lesion itself or to dysfunction of cortical language zones. A consecutive series of 25 right-handed stroke patients with left hemisphere lesions verified by CT scanning were examined for aphasia in the acccute stage, and two weeks, three months and six months after the insult. Cerebral angiography, CT scan and regional cerebral blood flow (rCBF) measurements with the 133Xe intracarotid method were performed in the acute stage. The CT scan was repeated six months later. Seven patients had lesions which involved cortical structures. All of these were severely aphasic in the acute stage and six months later. The rCBF studies showed severe reduction of flow in the infarcts; the perfusion was incompatible with tissue viability. Eighteen patients had subcortical lesions. Eight of these were mildly to severely aphasic in the acute stat. Recovery was always excellent. Five patients recovered completely, while 3 showed only discrete (clinically undetectable) aphasia after six months. The rCBF demostrated low-flow areas in the cortex overlying the deep lesions, with a blood flow which was sufficient for tissue viability, but insufficient for normal tissue function (an ‘ischaemic penumbra’). The blood flow was pressure dependent (showing impaired autoregulation) in these low flow areas. Ten patients with subcortical lesions were not aphasic. Their CBF was normal. The subcortical lesions were permanent on CT scan while aphasia was transient in these patients as recovery was seen within three months. It was therefore unlikely that the subcortical lesions as such were the cause of aphasia. The present findings indicate that aphasia in patients with subcortical lesions may be due to hypoperfusion and fuctional loss in cortical language zones. The cortical low-flow areas were invariably confined to occluded vascular territories. These territories were kept viable by collateral circulation characterized by penumbbral flow and impaired autoregulation. The patients showed excellent recovery from aphasia. We suggest that the recovery of language is caused by spontaneous arterial recanalization or expansions of collaterals, giving rise to enhancement of flow in the hypoperfused cortical penumbra.

Observations on the genesis of the stretch reflex in parkinson's disease

Abstract: Using surface electromyography the reflex response of flexor carpi radialis elicited by forcibly dorsiflexing the wrist was compared with that elicited by applying vibration percutaneously to its tendon. This was done both in patients with Parkinson's disease and in normal subjects. The reflexes were elicited on top of a pre-existing voluntary contraction of the muscle of about 20 per cent maximum. The responses in parkinsonism were qualitatively similar to the normal, but differed quantitatively in certain respects. The response to 'stretch' of the muscle by wrist dorsiflexion normally continued at a high level up to at least 80 ms from the beginning of the movement, commonly with an apparent separation into 'short' and 'long' latency responses. On average, the later components of the response were enhanced in parkinsonian patients in comparison with the normals, confirming other workers' findings; they were also prolonged. The short-latency responses were unchanged. Vibration, in contrast, elicited solely a short-latency response with the initial reflexly-evoked augmentation of EMG activity coming to an end 40 to 50 ms from the beginning of the stimulation, even though the vibration was continuing. Such an absence of the later components that were so prominent with stretch was found whatever the size of the initial short-latency response evoked by vibration, including when it was comparable to that evoked by stretch in the same subject. This purely short-latency vibration response was on average unchanged in parkinsonism. The findings support the hypothesis, already advanced for the long flexor of the thumb, that the long-latency components of response are largely attributable to a spinal excitatory action of the spindle group II afferents with the delay arising from the slowness of their conduction. They are not readily compatible with either of the two major alternative hypotheses, namely the 'long-loop' (or transcortical) hypothesis and the 'resonance' hypothesis, both of which attribute the late response, as well as the initial response, to the spindle Ia afferents. The enhancement of the later components of response in parkinsonism thus now seems likely to be due to an increase in the postulated spindle group II excitatory action, possibly related to a reduction in opposing inhibition, rather than to any change in the reflex excitability of the higher centres on Ia activation. However, the rigidity of parkinsonism cannot be uniquely ascribed to an enhancement of group II action, because over the population as a whole clinically similar degrees of rigidity could be accompanied by quite different long-latency responses, and vice versa.

Infarcts of both inferior parietal lobules with impairment of visually guided eye movements, peripheral visual inattention and optic ataxia.

Abstract: Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic adenocarcinoma The initial left-sided infarct induced right visual neglect, impairment of right-beating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OKN slow phase. The lesion on the left involved the upper part of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the SPL As the oculomotor deficits and the peripheral visual inattention were bilateral after the second infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres. The zone damaged in common included a small part of the SPL, the superoanterior extremity of the angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all visually guided eye movements and in visual attention It is further suggested that two corticofugal pathways are implicated in visually guided saccades, the first arising from the frontal eye fields and projecting directly onto the premotor structures in the brainstem, the second arising from the posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and including a relay in the superior colliculus before reaching the premotor structures Lastly, the findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed occipitofrontal pathways coursing in the deep white matter of the parietal lobe.

Cranial nerve ischaemic arterial syndromes

Abstract: Topographical vascular disorders involving combinations of cranial nerves are reviewed in this study. These are indicated by the correspondence between groupings of clinical manifestations and anatomical vascular distributions. Confirmatory evidence is provided by mishaps, following diagnostic or therapeutic angiography. Three systems play a role in the vascularization of cranial nerves: the inferolateral trunk (ILT), most often arising from the internal carotid artery, the middle meningeal system (MMS), and the ascending pharyngeal system (APS); the latter two are both derived from the external carotid artery. Conclusions concerning the ILT are least definite because of variations in vascular territory and the lack of confirmation from embolic events in a vascular region that is rarely the site of embolization. The specific ILT territory includes cranial nerve III and also nerves IV, VI and V1. Knowledge of the vascularization of nerve III may furnish explanations as to its different modes of involvement in diabetes mellitus. For the MMS, the cranial nerves concerned are V2, V3 and VII. Two vascular territories for the intrapetrous portion of nerve VII are defined: the first (stylomastoid artery) is limited to nerve VII; the second (MMS) supplies VII and V. Two examples of involvement of VII and V following selective MMS embolization are presented. A study of Bell's palsy associated with nerve V impairment is summarized. The APS supplies nerves IX, X, XI and XII; XI has a dual vascularization which explains why it can either be spared (as was the case in an angiographic accident) or involved (as in a case of herpes zoster). A vascular mechanism should be considered when cranial nerve lesions occur in the syndromes described here.

Movement deficits caused by hyperexcitable stretch reflexes in spastic humans

Abstract: SUMMARY Spastic patients were instructed to make accurate, rapid ankle dorsiflexion and plantarflexion movements over different distances to a target. Ankle position and surface electromyograms (EMGs) from tibialis anterior (TA) and soleus (SOL) muscles were recorded. In 3 of 8 spastic patients tested, dorsiflexion evoked velocity-dependent activation of the antagonist (SOL) muscle which impeded the movement to the extent that the limb unintentionally reversed movement direction. We propose that this activation is reflex in origin since it (1) is tightly synchronized, (2) has a large peak amplitude, (3) occurs about 50 ms after the initiation of the movement, and (4) is velocity dependent One of the 3 patients who had reflex-induced antagonist activation in dorsiflexion also demonstrated sustained clonus during plantarflexion. This usually occurred only if the target had been overshot so that the return of the limb stretched the soleus muscle and triggered clonus We conclude that in some patients, hyperactive stretch reflexes cause movement deficits.

Components of visual attention. Alterations in response pattern to visual stimuli following parietal lobe infarction.

Abstract: The contribution of attentional factors per se in response to visual stimuli was studied in patients with unilateral lesions of the left or right cerebral hemispheres. Subjects were required to respond to visual targets that were presented tachistoscopically, and were preceded by spatial cues that served to manipulate the spatial locus of attention. On 'valid' cue trials, the cue directed attention to the target's spatial coordinates; on 'invalid' cue trials, the cue misdirected attention. It was determined that damage to either the left or right hemisphere results in a general slowing of reaction times to visual stimuli irrespective of where such stimuli appear, and that patients with right parietal lesions are further impaired at shifting attention within the left visual field.

Mechanisms of unilateral spatial neglect in relation to laterality of cerebral lesions

Abstract: SUMMARY An Overlapping Figures test, considered as appropriate to study focusing of attention on small but complex stimuli falling in the central parts of visual field and a Searching for Animals test, designed to study the exploration of large parts of extrapersonal space, were administered to 38 controls, and 90 nght and 82 left brain-damaged patients. The investigation was designed to test the hypothesis that the extent of space to be explored may have a different influence on unilateral spatial neglect of right and left brain-damaged patients. Both right and left brain-damaged patients showed an asymmetric exploration of space on the Searching for Animals test, making more omissions on the side contralateral to the damaged hemisphere than on the ipsilateral one. On the Overlapping Figures test, however, only nght brain-damaged patients showed a clear tendency to omit figures lying on the left side of the composite pattern. This finding suggests that inability to extract visual information from one side of the stimuli dunng single eye fixatisons may be the most charactenstic feature of unilateral spatial neglect resulting from right hemisphere lesions.

Hypometria with hemispatial and limb motor neglect

Abstract: A patient with a haemorrhage in the right mesial frontal lobe exhibited hypokinesia, bradykinesia and a hypometric movement disorder of his contralateral limbs. This movement disorder was characterized by reduced amplitude of otherwise normally formed movements (hypometria). In addition, the left limb hypokinesia improved with placement of the left forelimb into right hemispace (hemispatial motor neglect). We postulate that the hypokinesia, bradykinesia and hypometria were induced by reduction in activation of forebrain dopaminergic and basal ganglion motor systems, which in conjunction with the supplementary motor area are critical for setting the activational level for motor output.

Viral infection in patients with multiple sclerosis and HLA-DR matched controls.

Abstract: Retrospective comparisons of the prevalence and age, where appropriate, of some childhood infectious illnesses and vaccinations, together with serological evidence for exposure to 16 viruses, many of which have previously been implicated in the aetiology of multiple sclerosis (MS) were made in 177 patients with acute optic neuritis, other recent isolated demyelinating episodes or established MS and 164 controls. The expected high frequency of HLA-DR2 in patients with demyelinating disease was matched by preselection of normal controls with this antigen (DR2+); the remaining individuals were classified as HLA-DR2 negative/DR3 positive (DR3+) or HLA-DR2 and 3 negative (DR2/3 -). Cases were compared with controls, collectively and in analyses restricted to each genetic group; these comparisons were repeated considering the three categories of patients with demyelination and two control populations separately. All DR2+, DR3+ and DR2/3 - individuals were compared in a single analysis to assess the effect of HLA type itself on the results. Patients with demyelinating disease had rubella and measles at a later age and reported mumps infection more frequently than controls. Age of typhoid vaccination and duration of exposure to domestic dogs was higher in all cases than controls. Age of measles and mumps, but not rubella, was higher in DR2+ cases than controls; but differences were not observed in the other genetic groups. Higher rubella antibody titres were present in all cases than controls and in analyses confined to DR2+ individuals in whom higher Epstein Barr virus antibody titres were also present. Measles haemagglutination inhibition and parainfluenza I antibody titres were increased and influenza A antibodies detected less frequently in all patients with optic neuritis and those with DR2 compared with appropriate controls; influenza B antibody titres were lower in all DR2+ cases than controls. Higher adenovirus and varicella zoster antibody titres were present in DR2/3- patients with demyelination and other neurological diseases compared with normal controls. Overall, older age of infection and higher antibody titres were observed more often in patients with optic neuritis, in particular DR2+ cases, than other individuals with demyelination or controls. Our serological results are consistent with the presence of abnormal HLA-immunological reactivity in patients with MS but cannot be explained only by an effect of DR type itself; age at which susceptible individuals develop some common childhood infections may also influence the subsequent development of the disease.

Infarction in the territory of the anterior choroidal artery. A clinical and computerized tomographic study of 16 cases.

Abstract: Sixteen cases of the anterior choroidal artery syndrome are reported. In its completed form, this rare syndrome combines the triad of hemiplegia, hemianaesthesia, and homonymous hemianopia. CT examination confirms the diagnosis by revealing an area of reduced density situated in the posterior limb of the internal capsule, sparing the thalamus medially and encroaching upon the tip of the globus pallidus laterally, and corresponding to the distribution of the anterior choroidal artery. Incomplete forms of the syndrome are more frequent. Left-sided spatial neglect may accompany right-sided lesions, as may slight disorders of speech in left-sided lesions. Clinical-anatomical correlations are discussed.