Newly diagnosed multiple sclerosis in state of Qatar.

BACKGROUND: Epidemiologic studies on multiple sclerosis (MS) are well-documented in the western population but to a lesser extent in Arab world. OBJECTIVE: To study the demographics, clinical aspects, radiologic and laboratory features along with the degree of disability inflicted, and factors affecting disease progression and outcome of newly diagnosed MS patients at our institution. METHODS: Data from all newly diagnosed MS patients fulfilling McDonald criteria from January 01, 2005 to December 31, 2010 were collected and analyzed. RESULTS: A total of 142 patients were identified, in which 82 (58%) were Qataris, and 90 (64%) females. Mean age was 31 years, and mean duration of symptoms was 24 days (median 15 days). Most common symptoms were sensory (63%), followed by visual (45%) and motor (43%). Mean EDSS was 2.3 at presentation. Treatment was given to 127 (89%), and relapse observed in 49%. Gadolinium enhancing lesions on follow-up MRI brain and relapsing remitting MS were associated with increased radiologic disease burden, while weakness at onset, EDSS of ≥2.5 and ≥3 clinical relapse was associated with clinical disease progression. CONCLUSION: MS in Qatar is an emerging disorder especially in the native population. The pattern of disease differs from other Middle Eastern countries by its milder clinical and aggressive radiologic disease presentation.

Tuberculoma of the brain: a series of 16 cases treated with anti-tuberculosis drugs.

OBJECTIVES: To describe the clinical presentation, radiological findings and outcome of treatment with antituberculosis drugs in 16 cases of intracranial tuberculoma. DESIGN: Consecutive cases admitted with tuberculoma to the National Center for Neurological Diseases in Khartoum, Sudan, were included in the study. The diagnosis was based on clinical and neuro-imaging features and response to anti-tuberculosis treatment. Histopathology of material from the brain or other extracranial tissues was available in seven cases. RESULTS AND CONCLUSIONS: The commonest presenting features were headache (100%), generalized convulsions (68.7%) and hemiparesis (56.2%). Computerised axial tomography/magnetic resonance imaging (CT/MRI) showed single or multiple lesions that showed intense contrast enhancement and perilesional edema. The lesions completely cleared on anti-tuberculosis treatment in the majority of survivors (13/15). Partial clearance of lesion was associated with late presentation, multiple large lesions and advanced miliary disease. We advocate early empirical trial of anti-tuberculosis drugs for intracranial tuberculoma even after a presumptive diagnosis, particularly in areas where the infection is endemic.

Pure isolated unilateral internuclear ophthalmoplegia from ischemic origin: report of a case and literature review.

PURPOSE: To report a case of pure isolated unilateral internuclear ophthalmoplegia from ischemic stroke, and to review its literature. METHODS: A 55-year old man, with a history of long-standing diabetes mellitus, developed acute-onset left internuclear ophthalmoplegia. MRI revealed a small paramedian dorsal pontine infarct ventral and lateral to the aquaductus cerebri. Intracranial MR angiography was normal. A systematic search was performed of the literature from January 1980 to December 2004 by using MEDLINE and EMBASE. Case reports with or series including patients with negative MRI findings were excluded. RESULTS: Nine cases of pure isolated MRI-proven unilateral INO resulting from ischemic stroke including this one, have been reported. In over 75% recovery was reported. CONCLUSION: Isolated unilateral internuclear ophthalmoplegia can be the sole manifestation of ischemic stroke and generally carries a good prognosis.

Stroke in Qatar: a one-year, hospital-based study.

BACKGROUND AND PURPOSE: Stroke is a major health problem in Qatar, yet no stroke studies have been reported from this region. This hospital-based study was conducted to determine the types and the 30-day fatality rate of stroke. The data were collected from the only hospital in Qatar and, therefore, are considered to be community-based estimations. METHODS: Clinical information was collected from discharge records of all patients with International Classification of Diseases, 9th Revision, (ICD 9) codes 430 to 438 from January 1 to December 31, 1997. Identification of cases included review of death certificates and brain computed tomography (CT) records for the same period. RESULTS: First-ever stroke was found in 217 patients (157 men and 60 women). The overall incidence rate was 41 per 100,000 inhabitants per year (95% CI, 30.2-52.4/100,000/year) and 238/100,000/year for the population over 45 years old. The age standardized incidence was 57.5 per 100,000 inhabitants per year (95% CI, 43.1-73.8). The crude incidence for native Qataris was 75 per 100,000 inhabitants per year. The mean age of patients experiencing their first stroke was 57 years. Thirty-nine (18%) patients were younger than 45 years. Clinical subtypes of stroke were ischemic (80%), intracerebral hemorrhage (19%), and subarachnoid hemorrhage (1%). Risk factors included hypertension (63%), diabetes mellitus (42%), ischemic heart disease (17%), and atrial fibrillation (4.5%). The overall patient fatality rate at 30 days was 16%. CONCLUSION: Stroke incidence in Qatar is lower than in other countries; a low incidence of subarachnoid hemorrhage was noted. The low mean age of stroke patients reflects the demographic characteristics of the population in Qatar. The high percentage of stroke patients suffering from hypertension and diabetes reflects the high prevalence of these risk factors in the population.

Post malaria cerebellar ataxia and ocular flutter: report of two cases.

We report two cases of post malarial cerebellar ataxia presenting with severe ocular flutter, in a female of 72 years and a male of 20 years. Both patients had falciparum malaria infection. CT scans of both patients were within normal limits for the age. Cerebellar signs as well as ocular flutter responded very well to moderate doses of prednisolone therapy.

Clinical presentation and CAT scan findings in mycetoma of the head.

Nine cases comprising seven males and two females with mycetoma of the cranium were studied between January 1990 and June 1997. Streptomyces somaliensis was the most common causative organism. The source of the infection was thought to be known in only three cases. The common mode of presentation was headache and scalp swelling. The next common presentation was epilepsy. Other focal neurological disorders also occur. CT scan findings of the cranium showed osteosclerotic rather than osteolytic changes.

Unusual neuropsychiatric manifestations of hypoparathyroidism: report of two cases.

Clinical, laboratory and radiological features of two cases of hypoparathyroidism presenting with pure neurological disease are described. The first patient has choreoathetosis and the second has mutism, locked jaw bilateral papilloedema and generalised tonic clonic epilepsy. Computerised tomography of the brain showed extensive calcification in the gray and white matter in both cases. Such combination of neurological manifestation of the disease and extensive cerebral calcification is rarely encountered and reported. It is concluded that brain calcification, which is generally believed to be asymptomatic, can cause frank neurological disease when it is extensive.

Motor neurone disease in the tropics: findings from Sudan.

In this clinical study the presentation, electromyography and nerve conduction studies were described in different types of motor neurone disease in 28 Sudanese patients seen at El Shaab and Khartoum Teaching Hospitals. The three major clinical subtypes encountered were amyotrophic lateral sclerosis (n = 19), progressive bulbar palsy (n = 7) and progressive muscular atrophy (n = 2). Family history of the disease was found in four patients and those mainly presented with bulbar symptoms. Sudanese patients were found to have an earlier age of onset and a better prognosis of the disease than their caucasian counterparts.

Post-malarial cerebellar ataxia in adult Sudanese patients.

In this study the clinical manifestation and the effect of corticosteroids on the course and the outcome of post malaria cerebellar ataxia on thirty adult Sudanese patients wr investigated. Twenty four patients with delayed ataxia, that is, ataxia occurring shortly after full recovery from otherwise uncomplicated, documented malaria and six patients who were found to be ataxic on recovery from cerebral malaria were included in the study. The distribution of the age, sex and various clinical aspects were outlined. Twelve randomly selected patients were given oral prednisolone. The corticosteroid was found to shorten the period of ataxia. It was also found that in patients who demonstrated cerebellar infarction or atrophy on computerised tomography the duration of ataxia was significantly long.

Oedema-related tissue damage after temporary and permanent occlusion of the middle cerebral artery.

Eleven adults spontaneously-hypertensive male rats (SHR) were studied 22 h or 7 days after a 2 h unilateral occlusion of the right middle cerebral artery (MCA). Another 11 SHR were studied after 24 h or 7 days of permanent MCA ligation. The brain infarcts were significantly larger (P < 0.05) after permanent occlusion than after a 2 h occlusion. More extensive and widespread vasogenic oedema, emanating from the infarcts, was visualized immunohistochemically in the temporarily-ligated animals and the relative number of astrocytes in their contralateral hemispheres was greater, thereby indicating that the vasogenic oedema influences the degree of gliosis. An immunopositivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where cytolytic nerve cell damage, severely shrunken and karyorrhectic nerve cells as well as gliosis were found one week after permanent and temporary MCA ligation. The histological changes in the thalamus indicated a difference in timing between lateral and medial parts of the lesion as well as between temporarily- and permanently-ligated SHR. These findings together with the close spatial correlation with albumin immunoreactivity indicate that the spread of extravasated plasma constituents or degradation products with the oedema bulk flow from the infarct influences the timing, character and extent of thalamic lesions after cerebral infarction.

The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction.

Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.

Parenchymal changes related to plasma protein extravasation in experimental seizures.

To determine whether the transient opening of the blood-brain barrier (BBB) during epileptic seizures may lead to permanent neuronal changes, seizures of a few minutes' duration were induced by intravenous (i.v.) administration of 0.3 mg/kg bicuculline to conscious rats with indwelling catheters for blood pressure (BP) and blood gas monitoring. The rats were killed 5 min to 7 days later, and the distribution of endogenous plasma albumin, fibrinogen, and fibronectin in the brain was studied by immunohistochemistry. Parallel sections were scrutinized for evidence of light-microscopic structural changes in the tissue. Extensive multifocal extravasation of plasma proteins throughout the brain and brainstem was observed. The original clearly focal distribution became more diffuse with prolongation of the recovery time. In addition, the intensity of the immunoreactivity decreased, most likely due to drainage into the cerebrospinal fluid (CSF) in the ventricles and the subarachnoidal space of the extravasated proteins, but some antialbumin-positive material was still visible after 7 days. In areas with extravasation, many nerve cells, especially cerebellar Purkinje cells, became strongly positive for albumin. In some of these areas, neurons appeared to be irreversibly injured. Thus, considerable amounts of plasma proteins are extravasated even during short epileptic seizures, and albumin appear to remain in the tissue for a long time, especially in Purkinje cells. The Purkinje cell loss in chronic epilepsy may be caused partly by cumulative bouts of plasma extravasations.

Regional cerebral blood flow in acute hypertension induced by adrenaline, noradrenaline and phenylephrine in the conscious rat.

Hypertension was induced in conscious rats by intravenous infusion of phenylephrine (3, 6 or 12 micrograms kg-1 min-1), noradrenaline (3 micrograms min-1) or adrenaline (3 micrograms kg-1 min-1). Local cerebral blood flow was measured autoradiographically in 24 defined brain structures using [14C]iodoantipyrine as the diffusible tracer. The mean arterial pressure induced by adrenaline, noradrenaline and the two higher doses of phenylephrine was 158-168 mmHg with no significant differences between the groups. Only adrenaline significantly increased local cerebral blood flow in nine of the 24 structures studied. The smaller capacity for autoregulation after adrenaline compared with other drugs might be related to a beta-adrenoreceptor-stimulating effect.

Endogenous serum albumin content in brain after short-lasting epileptic seizures.

Epileptic seizures can transiently alter the blood-brain barrier. We have determined the content of extravasated endogenous serum albumin in the brain and its change with time after bicuculline (0.3 mg/kg) induced epileptic seizures of a few minutes' duration in conscious rats. The brains were perfused with saline in situ 5 min, 2 h, 24 h, 3 or 7 days after the injection of bicuculline. The content of endogenous serum albumin in the cerebral cortex, diencephalon, mesencephalon, pons and cerebellum was determined by rocket immunoelectrophoresis. At 5 min the extravasation was most marked in the diencephalon with levels above 99% of the confidence limit of control brains in 8 out of 9 brains. Higher levels were seen at 2 h than at 5 min in the cerebral cortex and the cerebellum. Since it is known that the barrier rapidly normalizes after seizures, these findings suggest redistribution probably along clearance pathways into the cerebrospinal fluid (CSF) and possibly re-entry of albumin into the parenchyma from the CSF. Four out of 6 rats still had increased albumin levels in the cerebral cortex at 24 h. At 72 h and 7 days no values differed from controls.

Adrenaline-induced hypertension: morphological consequences of the blood-brain barrier disturbance.

Acute hypertension may transiently open the blood-brain barrier (BBB). To determine whether such temporary exposure of the brain parenchyma to plasma constituents may lead to permanent morphological alterations, acute hypertension was induced by i.v. adrenaline in conscious rates given Evan's blue and horseradish peroxidase as tracers. The brain were perfused in situ 24 h later: 17 of 21 brains showed multifocal sites of extravasation of the tracers and of endogenous plasma albumin, fibrinogen and fibronectin identified by immunohistochemistry. The proteins spread locally in the parenchyma and were taken up by neurons. Within the leaking sites in the cortex, hippocampus, thalamus and basal ganglia some shrunken and grossly distorted acidophilic neurons were present. Focal areas of sponginess were observed in the subpial and subependymal zones. Thus, a transient opening of the BBB may lead to neuronal damage.

A transient hypertensive opening of the blood-brain barrier can lead to brain damage. Extravasation of serum proteins and cellular changes in rats subjected to aortic compression.

A transient increase in blood pressure was induced in 15 male Sprague Dawley rats by clamping the upper abdominal aorta for 8-10 min. Three rats served as controls. The brains were fixed by perfusion 2 h or 7 days later. Evan's blue-albumin (EBA) was used for macroscopic evaluation of the blood-brain barrier (BBB) integrity. Extravasated plasma albumin, fibrinogen and fibronectin were demonstrated by immunohistochemistry on paraffin sections. Glial fibrillary acidic protein (GFAP) was visualized in the same way. Parallel sections were analyzed for possible parenchymal changes associated with the BBB breakdown. Multiple focal areas of BBB opening were seen in the brains of the three rats killed 2 h after the hypertensive episode. The plasma proteins were present in the vascular wall, extracellular space and within certain neurons. Shrunken acid fuchsin positive neurons were seen in some areas of extravasation. After 7 days, in 5 out of 12 rats a few local lesions with EBA leakage and positive immunostaining for plasma proteins were seen. Structurally these lesions were characterized by shrinkage, fuchsinophilia and disintegration of neurons and proliferation of astrocytes. Thus, a transient opening of the BBB by acute hypertension may lead to permanent tissue damage.