Haemorrhagic pure motor stroke

To describe the clinical characteristics of haemorrhagic pure motor stroke (PMS). Twelve patients with haemorrhagic PMS were identified. Haemorrhagic PMS accounted for 3.2% of all cases of pure motor hemiparesis ( n  = 380) and 3.3% of intracerebral haemorrhage ( n  = 364) entered in the database. When compared with PMS of ischaemic origin, patients with haemorrhagic PMS were more likely to be younger (62.2 vs. 75.2 years, P  = 0.003) and to have headache (33% vs. 6.3%, P  =0.007) and thalamus involvement (25% vs. 2.4%, P  = 0.005). Limb weakness (100% vs. 74.1%; P  = 0.03), involvement of the internal capsule (50% vs. 17.3%, P  = 0.012) and symptom free at discharge (25% vs. 3.7%, P  = 0.012) were significantly more frequent in patients with haemorrhagic PMS than in the remaining cases of haemorrhagic stroke, whereas nausea and vomiting (0% vs. 25.9%, P  = 0.03), altered consciousness (0% vs. 42.9%, P  = 0.001), sensory symptoms (8.3% vs. 46.9%, P  =0.007) and ventricular haemorrhage (0% vs. 26.1%, P  = 0.028) were significantly less frequent. Haemorrhagic PMS is a very infrequent stroke subtype. Headache at stroke onset may be useful sign for distinguishing haemorrhagic PMS from other causes of lacunar stroke. There are important differences between haemorrhagic PMS and the remaining intracerebral haemorrhages.     

Brachiofacial pure motor stroke.

Pure motor stroke is the commonest lacunar syndrome, but it may be associated with nonlacunar mechanisms of infarction. Pure motor brachiofacial weakness has been considered as a partial syndrome depending on a lacunar mechanism. We studied the correlations between stroke type, topography of infarction and etiology in 22 patients with pure motor brachiofacial weakness who were consecutively admitted to our stroke unit during a 10-year period. Seventeen patients had a small deep infarct, 4 had a cortical infarct in the superficial MCA territory and 1 had no specific lesion. The part of the cardiovascular risk factors was about 36% for smoking, 13% for diabetes mellitus, 60% for dyslipidemia and 40% for heart disease. Hypertension was present in 75% of our cases. None of the patients had a large artery stenosis on Doppler ultrasonography. We concluded that brachiofacial pure motor stroke is not always correlated to lacunar infarcts and may be due to a cortical infarct. MRI should be performed when brain CT is normal because of the implications it may have in management and therapy.     

Transcranial magnetic stimulation after pure motor stroke.

OBJECTIVES: The objective of this study was to assess the sensitivity of motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in demonstrating the possible subclinical impairment of the corticospinal pathway after recovery, in patients with a clinical history of pure motor stroke (PMS) due to a single lacunar infarct detectable by magnetic resonance imaging (MRI).METHODS: MEPs were recorded from the first dorsal interosseous muscle of 20 healthy subjects and 40 patients, 6 months or more after PMS onset. Patients were evaluated clinically by means of the NIH stroke scale, the Medical Research Council (MRC) scale and the Barthel Index. The patients with full hand strength recovery and the normal controls were also tested by means of the 9-hole peg test.RESULTS: Motor threshold (MT), MEP amplitude and central motor conduction time (CMCT) of the affected side were significantly different from those of the normal side and of the control subjects. MT, MEP amplitude and CMCT obtained after stimulation of the affected hemisphere were significantly correlated with the MRC scale values of the affected hand. Eighty-six percent of patients with persistent hand strength deficit showed MEP abnormalities. In 21 patients with complete clinical recovery, a significant increase in MT and decrease in MEP amplitude on the affected side were observed.CONCLUSIONS: After PMS, neurophysiological changes may persist despite complete clinical recovery. TMS represents a sensitive tool that enables to demonstrate objectively the clinical and subclinical impairment of the corticospinal pathway.     

Clinical study of 222 patients with pure motor stroke

The objective was to assess the frequency of pure motor stroke caused by different stroke subtypes and to compare demographic, clinical, neuroimaging, and outcome data of pure motor stroke with those of patients with other lacunar stroke as well as with those of patients with non-lacunar stroke. Data from 2000 patients with acute stroke (n=1761) or transient ischaemic attack (n=239) admitted consecutively to the department of neurology of an acute care 350 bed teaching hospital were prospectively collected in the Sagrat Cor Hospital of Barcelona stroke registry over a 10 year period. For the purpose of the study 222 (12.7%) patients with pure motor stroke were selected. The other study groups included 218 (12.3%) patients with other lacunar strokes and 1321 (75%) patients with non-lacunar stroke. In relation to stroke subtype, lacunar infarcts were found in 189 (85%) patients, whereas ischaemic lacunar syndromes not due to lacunar infarcts occurred in 23 (10.4%) patients (atherothrombotic stroke in 12, cardioembolic stroke in seven, infarction of undetermined origin in three, and infarction of unusual aetiology in one) and haemorrhagic lacunar syndromes in 10 (4.5%). Patients with pure motor stroke showed a better outcome than patients with non-lacunar stroke with a significantly lower number of complications and in hospital mortality rate, shorter duration of hospital stay, and a higher number of symptom free patients at hospital discharge. After multivariate analysis, hypertension, diabetes, obesity, hyperlipidaemia, non-sudden stroke onset, internal capsule involvement, and pons topography seemed to be independent factors of pure motor stroke in patients with acute stroke. In conclusion, about one of every 10 patients with acute stroke had a pure motor stroke. Pure motor stroke was caused by a lacunar infarct in 85% of patients and by other stroke subtypes in 15%. Several clinical features are more frequent in patients with pure motor stroke than in patients with non-lacunar stroke.     

Basilar branch disease presenting with progressive pure motor stroke

Objectives - Isolated infarcts of the pons cause well definable neurological syndromes with distinct pathomechanism, clinical course and prognosis. Patients and results - We report 8 cases suffering from a pure motor hemiparesis that was severely progressive within the 1st 3 days and unresponsive to aspirin. A relatively good recovery was observed in all patients, however, stroke recurrence occurred in 2 cases within 3 months and resulted in pseudobulbar paralysis and tetraparesis. MRI displayed unilateral ( n =6) and bilateral ( n =2) ventromedial pontine infarctions (VPI). Angiographic evaluation ( n =4) or color Duplex examination ( n =4) revealed atherosclerotic lesions but no basilar artery occlusion. Conclusion - Although VPI due to basilar branch disease may clinically mimic a classical lacunar syndrome, it is related to a particular pathogenetic mechanism different from microangiopathy or embolism. In contrast to the MRI feature of lacunes, VPI typically extend to the basal surface of the pons. The progressive pattern, ending up in a relative uniform clinical picture, is probably caused by propagating thrombosis.     

Diffusion-weighted MRI diagnosis of pure motor stroke limited to primarily distal leg weakness.

Pure motor stroke (PMS) manifesting as distal weakness of a single extremity has rarely been described. The authors report a 59-year-old man with PMS who had primarily distal weakness of a single lower extremity, which to the authors' knowledge has not been previously described. Four days after onset, positive diffusion-weighted imaging confirmed that the small subcortical T2-weighted hyper-enhancing and nonenhancing T1-weighted hypo-intensity noted on magnetic resonance imaging (MRI) represented an acute PMS that was the cause of the patient's weakness. Increased awareness of this rare clinical presentation of PMS coupled with the promise of imaging the PMS with diffusion-weighted MRI should lead to earlier stroke intervention in these patients.     

Spastic pure motor monoparesis

Pure motor hemiplegia (PMH) is, in most cases, caused by a lacunar infarction. However, pure motor monoparesis (PMM), i.e., isolated motor involvement with spasticity in one limb, has drawn little attention. We studied prospectively 5 patients with PMM and found that it was always due to a mass lesion in the contralateral superficial cerebral hemisphere. Our observation suggests that PMM should not be regarded as simply a variant of PMH.     

Neurocysticercosis and pure motor hemiparesis

A 49-year-old man with meningeal cysticercosis presented with a pure motor hemiparesis. Computed tomography and magnetic resonance imaging showed a capsular infarction and a suprasellar cyst with surrounding arachnoiditis. Cerebrospinal fluid analysis confirmed the diagnosis as it showed positive immunologic reactions to cysticerci. This is the first reported case of pure motor hemiparesis due to a parasitic disease of the central nervous system.     

Circulating endothelial cells in acute ischaemic stroke

Increased numbers of CD146-bearing circulating endothelial cells (CECs) in the peripheral blood probably represent the most direct evidence of endothelial cell damage. As acute ischaemic strokes are associated with endothelial abnormalities, we hypothesised that these CECs are raised in acute stroke, and that they would correlate with the other indices of endothelial perturbation, i.e. plasma von Willebrand factor (vWf) and soluble E-selectin. We studied 29 hypertensive patients (19 male; mean age 63 years) who presented with an acute stroke and compared them with 30 high risk hypertensive patients (21 male; mean age 62 years) and 30 normotensive controls (16 male; mean age 58 years). CECs were estimated by CD146 immunobead capture, vWf and soluble E-selectin by ELISA. Patients with an acute ischaemic stroke had significantly higher numbers of CECs/ml of blood (p<0.001) plasma vWf (p=0.008) soluble E-selectin (p=0.002) and higher systolic blood pressure (SBP) as compared to the other groups. The number of CECs significantly correlated with soluble E-selectin (r=0.432, p<0.001) and vWf (r=0.349, p=0.001) but not with SBP (r=0.198, p=0.069). However, in multivariate analysis, only disease group (i.e. health, hypertension or stroke) was associated with increased CECs. Acute ischaemic stroke is associated with increased numbers of CECs. The latter correlate well with established plasma markers of endothelial dysfunction or damage, thus unequivocally confirming severe vasculopathy in this condition. However, the greatest influence on CECs numbers was clinical group.     

Role of endogenous testosterone concentration in pediatric stroke

Previous studies have indicated a male predominance in pediatric stroke. To elucidate this gender disparity, total testosterone concentration was measured in children with arterial ischemic stroke (AIS; n = 72), children with cerebral sinovenous thrombosis (CSVT; n = 52), and 109 healthy controls. Testosterone levels above the 90th percentile for age and gender were documented in 10 children with AIS (13.9%) and 10 with CSVT (19.2%), totaling 16.7% of patients with cerebral thromboembolism overall, as compared with only 2 of 109 controls (1.8%; p = 0.002). In multivariate analysis with adjustment for total cholesterol level, hematocrit, and pubertal status, elevated testosterone was independently associated with increased disease risk (odds ratio [95% confidence interval]: overall = 3.98 [1.38–11.45]; AIS = 3.88 [1.13–13.35]; CSVT = 5.50 [1.65–18.32]). Further adjusted analyses revealed that, for each 1nmol/l increase in testosterone in boys, the odds of cerebral thromboembolism were increased 1.3‐fold. Ann Neurol 2009;66:754–758     

Computed tomography and pure motor hemiparesis

Computed tomography (CT) was abnormal in 75% of 33 patients with pure motor hemiparesis (PMH). In 13 cases, lesions were detected in the capsular region; 10 were consistent with infarction, and 3 were of increased density consistent with hemorrhage. Seven had other vascular disorders, and four had nonvascular conditions. Of 20 patients with PMH with normal electroencephalogram (EEG), isotope scan, and cerebrospinal fluid, 11 had CT evidence of a lesion in the internal capsule-corona radiata region. In patients with PMH with normal CT, recovery was more complete and rapid than in those with CT evidence of a vascular lesion. In 5 cases, CT showed a capsular lesion, although the patients had never had any neurologic deficit.     

Electrophysiological diagnosis of motor neuron disease and pure motor neuropathy

Motor neuron disease (MND) is a group of disorders in which there is degeneration of upper and lower motor neurons to a variable degree. Amyotrophic lateral sclerosis is the most frequent form of the disease, presenting with both upper and lower motor neuron involvement. Frequently, especially in the early stages of the disease, only lower motor neuron signs are present. In these conditions, some pure motor neuropathies may resemble MND. The diagnosis is of importance because some of these motor neuropathies are “dysimmune” disorders and may respond to immune therapies. In such diseases the multifocal motor neuropathy with conduction block appears to be the more frequent. In MND and pure motor neuropathies, the electrophysiological examination is the most decisive test. In MND, it is of diagnostic importance. In addition, it is useful in the assessment of disease severity and progression, in the evaluation of therapeutic trials and in the understanding of etiopathogenesis of the disease. In pure motor neuropathies, the presence of conduction block leads to immune treatment with good response in more than 50% of the cases. Received: 20 August 1998 Accepted: 10 October 1998     

Capsular infarcts: location, size and etiology of pure motor hemiparesis, sensorimotor stroke and ataxic hemiparesis

We investigated the types of syndrome, location, size and presumed causes of 72 patients with acute capsular lacunar infarction. Clinical syndromes were classified into pure motor hemiparesis (PM), sensorimotor stroke (SM) and ataxic hemiparesis (AH). Lesion sizes of AH were significantly smaller than those of PM (p<0.01) or SM (p<0.01). When the lesion volume was classified into two groups, ≥ 1 ml and < 1 ml, the large volume group had more frequent cardioembolic sources than the small volume group (41% and 18% respectively, p<0.05). In AH patients no cardioembolic sources could be detected. Significant carotid stenosis was found in only 4% of patients. Patients with anterior choroidal artery territory infarction had infrequent cardioembolic sources (7%). The results suggest that the lesion size varies with clinical syndrome and some etiological trends are seen in the volume and the location of lesions.     

Imaging motor recovery after stroke

Most patients show improvement in the weeks or months after a stroke. Recovery is incomplete, however, leaving most with significant impairment and disability. Because the brain does not grow back to an appreciable extent, this recovery occurs on the basis of change in function of surviving tissues. Brain mapping studies have characterized a number of processes and principles relevant to recovery from stroke in humans. The findings have potential application to improving therapeutics that aim to restore function after stroke.     

Human immunodeficiency virus-associated pure motor lumbosacral polyradiculopathy

BACKGROUND: Neuromuscular disease is a common manifestation of human immunodeficiency virus infection and acquired immunodeficiency syndrome, but isolated and severe pathology confined to the motor roots or anterior horn cells are not a recognized clinical entity. OBJECTIVE: To describe the novel clinical presentation of human immunodeficiency virus-related polyradiculopathy manifesting as isolated severe motor symptoms confined to the legs. DESIGN: A case series comprising 4 patients identified prospectively during a 6-month period. SETTING: Patients were seen in the Department of Neurology, Groote Schuur Hospital, Cape Town, South Africa. This is an 800-bed teaching hospital, with approximately 5000 patients seen annually in the Department of Neurology. PATIENTS: Patients were identified by their unique presentation with a severe isolated motor neuropathy in the lower limbs. All were Xhosa-speaking African women. RESULT: Early human immunodeficiency virus infection may be associated with pure motor lumbosacral polyradiculopathy. CONCLUSION: It remains unclear whether this clinical syndrome should be regarded as a variant of the Guillain-Barre syndrome or whether it represents a unique disorder associated with early human immunodeficiency virus infection.     

Putaminal haemorrhage leading to pure motor hemiplegia

Pure motor hemiplegia (PMH) is commonly attributed to lacunar infarction of internal capsule or basis pontis. We report 7 patients of pure motor hemiplegia as a result of small or moderate size putaminal haemorrhage. All the patients had normal median somatosensory evoked potentials. Central Motor Conduction Time (CMCT) to upper limb was not recordable in all 3 patients with complete hemiplegia. Three of seven patients had complete and four had partial recovery. Anterioposterior extension of small or moderate size putaminal haemorrhage seems to spare the medially located sensory fibres in the internal capsule. On the basis of our results, lateral putaminal haemorrhage should be considered in the differential diagnosis of PMH.     

A case of pure trigeminal motor neuropathy

We reported a case of pure trigeminal motor neuropathy. A 57-year-old man was admitted with the complaints of vague headache and left upper limb numbness. Neurological examination showed mild wasting of the right masseter muscle on chewing. The jaw deviated to the right when he opened his mouth fully. Corneal reflex was intact bilaterally and so was the sensation on the face and taste. Mild hemiparesis including the face was observed on the left. Laboratory data including cerebrospinal fluid analysis were normal except for mild glucose intolerance. Blink reflex, brainstem auditory response and trigeminal sensory evoked potential elicited by electric stimulation of the lower lip were all normal. EMG findings obtained from the left masseter and lateral pterygoid muscles were neurogenic. The CT scan demonstrated a characteristically distributed low density area, which substituted the muscle supplied by the motor branch of he trigeminal nerve, namely, the right masseter, temporalis, lateral and medial pterygoid muscles. With MRI, the lesion was high on T1 and T2 weighted images. In addition, spotty high signal intensities suggestive of small infarction were observed in the bilateral centrum semiovale on T2 weighted images. Judging from the above results, the present case was believed to have pure motor trigeminal neuropathy confirmed by electrophysiological findings and image analyses together with clinical features. The mild left hemiparesis was thought to be incidental complication of vascular origin.