Diagnostic pitfalls in stereotactic biopsy

Between October 1998-August 2000, 65 patients were diagnosed, and underwent stereotactic biopsy of brain lesions. Procedures were performed with the Riechert-Mundinger stereotactic device. The diagnosis was made intra-operatively, by examination of cytological smears. The initial diagnosis was confirmed after H&E, and selective stains, as well as immunohistochemical examinations of paraffin specimens. The method applied makes possible to obtain a reliable, and precise morphological diagnosis in the majority of cases, so that a proper treatment method could be introduced.     

Decompressive hemicraniectomy in ischaemic stroke

Background and purposeHemispheric ischaemic stroke complicated by oedema is associated with high mortality. The results of randomized studies showed that decompressive hemicraniectomy performed in this group of patients could be beneficial. First experiences with implementation of hemicraniectomy in patients with brain infarct in our stroke centre are presented.Material and methodsBetween August 2007 and July 2008, four patients with hemispheric brain infarcts complicated by malignant oedema underwent decompressive hemicraniectomy within 72 hours from symptoms onset. Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Clinical outcome was assessed 3, 6 and 12 months after the event using the modified Rankin scale (mRS).ResultsIn the first patient, the neurosurgical procedure included only decompressive hemicraniectomy, whereas in the other three duraplasty was performed additionally. The first patient died 23 days after the stroke onset due to acute respiratory failure. Another died at four months after the event, due to infectious complications. The remaining two patients presented severe functional disability 12 months after the procedure (mRS score 4).ConclusionsDecompressive surgery with duraplasty can be a life-saving procedure for patients with brain oedema. To our knowledge, the presented cases are among the first reported cases of hemispheric ischaemic stroke treated with decompressive hemicraniectomy in Poland. Extended follow-up with a larger group of patients is necessary to assess long-term outcome.     

Hyperbilirubinaemia in acute ischaemic stroke

Liver function tests were studied in 73 patients with acute ischaemic cerebrovascular events and were compared with those in a group of 63 control subjects with a similar age and sex distribution.     

Inflammation and ischaemic stroke

PURPOSE OF REVIEW: Inflammation is implicated in ischaemic stroke as a general cardiovascular risk factor, a possible immediate trigger, a component (and possible exacerbating factor) of the response to tissue injury, a marker of future risk, and as a therapeutic target. Each aspect is reviewed. RECENT FINDINGS: Evidence of epidemiological association of inflammatory markers, particularly C-reactive protein, has accrued, but the independence of inflammation from more conventional risk indicators is under question. Other inflammatory markers are associated with intermediate phenotypes such as hypertension. Tissue inflammation in atherosclerotic plaque is of probable relevance in identifying recently symptomatic carotid disease. Both humoral and cellular inflammation are evident following stroke, with evidence that these responses may exacerbate tissue injury. Blockade of interleukin-1, or of neutrophil chemotaxis, has reduced infarct volume in models of stroke but has yet to show benefit in clinical trials. Other anti-inflammatory strategies are promising. SUMMARY: Inflammation is implicated in several aspects of acute ischaemic stroke. It remains to be established whether the inflammatory response is a truly independent risk factor in general, or whether specific anti-inflammatory interventions are beneficial either in prevention or acute treatment.     

Genetics of ischaemic stroke

Ischaemic stroke is a heterogeneous multifactorial disorder. Epidemiological data provide substantial evidence for a genetic component to the disease, but the extent of predisposition is unknown. Large progress has been made in single-gene disorders associated with ischaemic stroke. The identification of NOTCH3 mutations in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) has led to new insights on lacunar stroke and small-vessel disease. Studies of sickle-cell disease have drawn attention to the importance of modifier genes and of gene-gene interactions in determining stroke risk. They have further highlighted a potential role of genetics in predicting stroke risk. Little is known about the genes associated with complex multifactorial stroke. There are probably many alleles with small effect sizes. Genetic-association studies on a wide range of candidate pathways, such as the haemostatic and inflammatory system, homocysteine metabolism, and the renin-angiotensin aldosterone system, suggest a weak but significant effect for several at-risk alleles. Genome-wide linkage studies in extended pedigrees from Iceland led to the identification of PDE4D and ALOX5AP. Specific haplotypes in these genes have been shown to confer risk for ischaemic stroke in the Icelandic population, but their role in other populations is unclear. Advances in high-throughput genotyping and biostatistics have enabled new study designs, including genome-wide association studies. Their application to ischaemic stroke requires the collaborative efforts of multiple centres. This approach will contribute to the identification of additional genes, novel pathways, and eventually novel therapeutic approaches to ischaemic stroke.     

Treatment of ischaemic stroke

Stroke is a neurological emergency that requires rapid diagnostic workup and immediate treatment. Basic medical management such as maintenance of a high level of systemic blood pressure, provision of an optimal supply of oxygen, and correction of hyperthermia, hyperglycaemia and hypovolemia can contribute to a more favourable clinical outcome of stroke patients. Neuroprotective drugs have shown to be effective in reducing cerebral infarct size in several animal species but their clinical benefit in stroke patients remains to be proven. Neither heparin nor aspirin can improve neurological outcome or significantly reduce death or dependency several months after the ischaemic event, but aspirin is clearly effective in reducing early death or stroke recurrence within the first few weeks. Early anticoagulation should be used for patients at high risk for recurrent cardioembolic stroke and with carotid or vertebral artery dissection, although this recommendation is not based on the results of randomised controlled trials.     

Diagnostic pitfalls in carpal tunnel syndrome

Background

This review focuses on the main aspects of positive and differential diagnosis of carpal tunnel syndrome (CTS) in different clinical situations encountered in daily practice.

State of the art

Authentic CTS can be discovered in situations, which alter the usual presentation or therapeutic management. This is the case for instance in pregnant women or in the elderly subject or with acute motor forms where CTS discloses a focal intratunnel disorder (neuroma, lipoma, arterial condition, bone disorder) or a general disease (hereditary neuropathy, amylosis). In certain situations, the clinical manifestations suggest a more proximal compression of the medial nerve (round pronator, Struthers arcade, or superficial flexor) or an inflammatory condition (mononeuritis, inflammatory demyelinising neuropathy). Locoregional disease may also be involved, for instance a plexus (thoracobrachial outlet syndrome, post-radiation plexitis) or radicular condition. The clinical presentation of diffuse polyneuropathy with initial manifestations involving the upper limb (ganglioneuropathies, polyradiculoneuritis, small-fiber neuropathies) may also be misleading. Finally central conditions can sometimes be confused with CTS.

Conclusion

A rigorous physical examination and an electroneuromyogram are determining to avoid diagnostic pitfalls.     

Delayed hypothermia in malignant ischaemic stroke

Moderate hypothermia may reduce mortality in malignant brain infarction. However, due to the extremely limited number of patients treated, it is still unknown whether it may be beneficial if undertaken several days after acute stroke, when the probability of a malignant oedema is higher. We report on a patient with malignant brain oedema after middle cerebral artery infarction, who was treated with moderate hypothermia on the third day after stroke when he became comatose. Hypothermia was induced at a rate of 1.25°C/h by an intravascular cooling catheter. The target temperature of 32°C was reached in about 6 h. After 36 h of hypothermia, the patient was actively re-warmed at a rate of 0.2°C/h. The patient survived and showed a progressive reduction of mass effect on CT scan. This single case study suggests a beneficial effect of hypothermia in the treatment of severe space-occupying ischemic infarction even on the third day after stroke onset.     

Outcome after ischaemic stroke in childhood

A parental questionnaire was used to investigate the outcome for children who had had ischaemic stroke, who were seen at Great Ormond Street Hospital, London between 1990 and 1996. The results of functional assessments carried out by a physiotherapist and an occupational therapist, and of quantitative evaluations carried out by a neuropsychologist were used for validation where possible. The relationship between clinical and radiological factors and outcome were examined. The children were aged between 3 months and 15 years at the time of stroke (median age 5 years) and the period of follow-up ranged from 3 months to 13 years (median duration 3 years). Of the 90 children for whom data were obtained, 13 (14%) had no residual impairments. Outcome was good in 37 children (40%) and poor in 53 (60%) (defined according to whether impairments interfered with daily life). Agreement, as measured by Cohen's kappa, was good or very good between the parents' responses and the qualitative measures provided by the medical professionals and the therapists, but only fair to moderate for the quantitative measures provided by the neuropsychologists. This may reflect different parental perceptions of the physical and cognitive aspects of outcome. Younger age at time of the stroke was the only significant predictor of adverse outcome.     

Prothrombotic abnormalities in childhood ischaemic stroke

Childhood ischaemic stroke, incorporating arterial ischaemic stroke and cerebral sinus venous thrombosis, is associated with significant morbidity and mortality in children. The majority of cases in children present with well-recognised risk factors.The appreciation of the role prothrombotic abnormalities have in disease states is developing rapidly. Prothrombotic abnormalities are abnormalities of the coagulation system, fibrinolytic system, endothelial cells or platelets that lead to a reduced threshold for pathological thrombus formation. Our understanding of the role of prothrombotic abnormalities in childhood ischaemic stroke is increasing and has a direct bearing on the development of effective management and prevention strategies.We provide a brief background of prothrombotic abnormalities and review the available literature on prothrombotic markers in childhood ischaemic stroke. Overall, prothrombotic abnormalities have been identified in 20-50% of children presenting with AIS and 33-99% of children with cerebral sinus venous thrombosis. There appear to be a number of associations emerging including an increased frequency of factor V Leiden mutation, elevated lipoprotein (a), protein C deficiency and antiphospholipid antibodies in children presenting with arterial ischaemic stroke. The pathogenic role of prothrombotic abnormalities as predisposing to initial and recurrent childhood ischaemic stroke is becoming increasingly evident. The impact on treatment, however, will only be clarified with carefully designed, multi-institutional prospective studies.