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The frequency of cerebellar infarctions over two and a half years was 2.7% of the 1300 hospitalized patients over that period. Sixteen patients with cerebellar infarctions were studied by using clinical manifestations and magnetic resonance imaging (MRI). Ages ranged from 41-87 (mean 63.5) years; 13 were men and 3, women. Risk factors included: hypertension (50%), diabetes (44%), prior stroke (44%), cardiac disease (38%), and hyperlipidemia (19%). Common symptoms and signs were dizziness/vertigo (75%), unsteadiness (69%), dysarthria (69%), and nausea/vomiting (50%). Infarcts mainly involved the posterior inferior cerebellar artery (PICA) territory and tended to be associated with brainstem infarcts in 14 of the 16 patients. Most cerebellar infarctions had a benign course, especially the small ones. No mortality was noted in this series. The short-term outcome of the cerebellar infarctions seemed to depend on the size of the infarcts and the sites of the artery occlusion. It was concluded that diagnosis of cerebellar infarctions requires a high index of clinical suspicion, especially when patients present with a sudden onset of ataxia, dizziness/vertigo, nausea/vomiting and dysarthria; and that MRI is a useful tool for the detailed study of cerebellar infarctions and can elucidate associated brainstem infarcts.
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PMID:A clinical and MRI study of cerebellar infarctions. 829 26

The cerebroprotective effect of the non-N-methyl-D-aspartate antagonist, NBQX (2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)-quinoxaline.NA) on neurological deficit and infarct volume (visualised with 2,3,5-triphenyltetrazolium) 24 h after permanent middle cerebral artery (MCA) occlusion in Fischer rats (n = 6 per dose) was studied. NBQX (10, 20 or 30 mg Kg-1, i.p., 0,30,60 min) immediately after MCA occlusion reduced cortical infarct volume by 45% (not significant), 70% (p < 0.05) or 75% (p < 0.05) respectively. NBQX (30 mg Kg-1, i.p., 60, 90, 120 min) reduced cortical infarct volume by 58% (p < 0.05). With a 2 h delay NBQX was ineffective. Neurological deficits (with blinded assessment) were improved with immediate or delayed NBQX (3 x 30 mg Kg-1, i.p.). The main adverse behavioral effect of NBQX (3 x 20 or 3 x 30 mg Kg-1, p.i.) was ataxia. The cerebroprotective effect of NBQX in rats suggests a possible therapeutic role for non-N-methyl-D-aspartate antagonists given shortly after stroke onset.
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PMID:Cerebroprotective effect of a non-N-methyl-D-aspartate antagonist, NBQX, after focal ischaemia in the rat. 833 Jul 53

We report a 57-year-old man who developed Wallenberg syndrome and vertebral artery dissection, probably as a complication of neck rotation during golf exercise. He noticed pain in the neck during golf exercise. About 16 hours later, he developed numbness in the right hand, cold sweat, vertigo, hiccup, double vision and ataxia in gait. Neurological examination on the 22nd day revealed a right Wallenberg syndrome. The right vertebral angiogram showed a marked stenosis of the vertebral artery at the portion across the dura, and a dissecting aneurysm in the portion from its entrance into the posterior fossa through the exit of the right posterior inferior cerebellar artery. Quick rotation and/or extension of the neck and head during golf exercise probably caused the vertebral artery dissection, resulting in Wallenberg syndrome. More attention should be paid to relatively trivial trauma as the cause of stroke, especially in the victims of younger ages.
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PMID:[Wallenberg syndrome and vertebral artery dissection probably due to trivial trauma during golf exercise]. 833 99

The mitochondrion is the only extranuclear organelle containing DNA (mtDNA). As such, genetically determined mitochondrial diseases may result from a molecular defect involving the mitochondrial or the nuclear genome. The first is characterized by maternal inheritance and the second by Mendelian inheritance. Ragged-red fibers (RRF) are commonly seen with primary lesions of mtDNA, but this association is not invariant. Conversely, RRF are seldom associated with primary lesions of nuclear DNA. Large-scale rearrangements (deletions and insertions) and point mutations of mtDNA are commonly associated with RRF and lactic acidosis, e.g. Kearns-Sayre syndrome (KSS) (major large-scale rearrangements), Pearson syndrome (large-scale rearrangements), myoclonus epilepsy with RRF (MERRF) (point mutation affecting tRNA(lys) gene), mitochondrial myopathy, lactic acidosis, and stroke-like episodes (MELAS) (two point mutations affecting tRNA(leu)(UUR) gene) and a maternally-inherited myopathy with cardiac involvement (MIMyCa) (point mutation affecting tRNA(leu)(UUR) gene). However, RRF and lactic acidosis are absent in Leber hereditary optic neuropathy (LHON) (one point mutation affecting ND4 gene, two point mutations affecting ND1 gene, and one point mutation affecting the apocytochrome b subunit of complex III), and the condition associated with maternally inherited sensory neuropathy (N), ataxia (A), retinitis pigmentosa (RP), developmental delay, dementia, seizures, and limb weakness (NARP) (point mutation affecting ATPase subunit 6 gene). The point mutations in MELAS, MIMyCa, and MERRF, and the large-scale mtDNA rearrangements in KSS and Pearson syndrome have a broader biochemical impact since these molecular defects involve the translational sequence of mitochondrial protein synthesis. The nuclear defects involving mitochondrial function generally are not associated with RRF. The biochemical classification of mitochondrial diseases principally catalogues these nuclear defects. This classification divides mitochondrial diseases into five categories. Primary and secondary deficiencies of carnitine are examples of a substrate transport defect. A lipid storage myopathy is often present. Disturbances of pyruvate or fatty acid metabolism are examples of substrate utilization defects. Only four defects of the Krebs cycle are known: fumarase deficiency, dihydrolipoyl dehydrogenase deficiency, alpha-ketoglutarate dehydrogenase deficiency, and combined defects of muscle succinate dehydrogenase and aconitase. Luft disease is the singular example of a defect in oxidation-phosphorylation coupling. Defects of respiratory chain function are manifold. Two clinical syndromes predominate, one involving limb weakness, and the other primarily affecting brain function. Leigh syndrome may result from different enzyme defects, most notably pyruvate dehydrogenase complex deficiency, cytochrome c oxidase deficiency, complex I deficiency, and complex V deficiency associated with the recently described NARP point mutation. A new group of mitochondrial diseases has emerged.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The expanding clinical spectrum of mitochondrial diseases. 833 7

A patient with rheumatoid arthritis on immunosuppressive therapy was admitted to hospital with the sudden onset of diplopia and ataxia. Because of the history, a stroke was thought most likely. However, as he progressed a diagnosis of the Miller Fisher syndrome was established. He responded to plasma exchange. This presentation is highly unusual and has not previously been described. In addition, the possibility of immune dysregulation setting the stage for the development of this syndrome is discussed. The role of plasma exchange for this condition is also reviewed.
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PMID:Miller Fisher syndrome mimicking stroke in immunosuppressed patient with rheumatoid arthritis responding to plasma exchange. 834 Apr 81

We describe a 42-year-old woman with overlapping syndrome of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and MERRF (myoclonus epilepsy and ragged-red fibers). Clinically, she had episodic headache, stroke-like episode with left hemiparesis and lactic acidosis commonly found in MELAS syndrome. However, myoclonus seizure, and ataxia with dyssynergic gait characteristic of MERRF were also noted. Computed tomographic scans showed a right temporo-parietal hypodense lesion. The lesion disappeared 20 months later, even magnetic resonance images also failed to reveal this abnormality. A molecular analysis of mitochondrial DNA was conducted by using restriction endonucleases ApaI and NaeI. A transition from A to G was found at the nucleotide position 3243, but not found at the 8344th nucleotide pair. In this report, we document the fluctuating CT changes and emphasize the importance of molecular analysis in patients with overlapping syndrome of mitochondrial encephalomyopathies.
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PMID:Overlapping syndrome of MERRF and MELAS: molecular and neuroradiological studies. 835 81

CNS manifestations appear in one of 1,000 patients with Mycoplasma pneumoniae-associated infections. Encephalitis is the most frequent manifestation, but cases of meningitis, myelitis, and polyradiculitis, as well as many other symptoms (e.g., coma, ataxia, psychosis, and stroke), have been reported. The onset of these manifestations is usually acute, with lowered consciousness, convulsions, pareses, and other neurological signs. Severe, even fatal, cases are known. The pathophysiology of CNS manifestations is unknown. To our knowledge, M. pneumoniae has never been isolated from brain tissue, but instead it has been recovered from CSF specimens in at least seven cases. Besides direct invasion of M. pneumoniae into the brain, neurotoxic or autoimmune reaction within the brain tissue is suspected. At neuropathological examination, edema, demyelination, and microthrombi have been described. Improved diagnostic methods may reveal the pathophysiology of CNS manifestations associated with M. pneumoniae infection.
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PMID:CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. 839 38

A 15 year-old boy developed meningoencephalitis two weeks after onset of a respiratory tract infection caused by Mycoplasma pneumoniae. Central nervous complications are seen in 2-7% of patients hospitalized for M pneumoniae infection. Meningoencephalitis, meningitis, ataxia, polyradiculitis, psychosis and a few cases of apoplexy have been reported. In clinical practice one should be aware of M pneumoniae in the differential diagnosis of patients with suspected microbiologically induced central nervous complications. The pathogenetic aspects and prognosis are briefly discussed.
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PMID:[Meningoencephalitis after Mycoplasma pneumoniae infection]. 846 13

Twenty-five patients with various types of gait disorders of multi-infarct dementia (MID) were reported. The types of gait disorders consisted of lower body parkinsonism (LBP) plus ataxia (6 patients), LBP plus apraxia (5 patients), and a combination of LBP plus ataxia and apraxia (14 patients). Hypertension occurred in 23 (92%) of the 25 patients. Nevertheless, individual stroke risk factors and the locations of infarcts were not significantly different between the subgroups. Ventriculomegaly and "leuko-araiosis" as demonstrated by computed tomography occurred in more than 80% of patients in each subgroup. Atrophy of the superior vermis was seen in 16 (80%) of 20 patients with ataxia as compared to 2 (40%) of the 5 patients without ataxia (p < 0.005). These data suggest that LBP and apraxia of MID were probably determined by the presence of ventriculomegaly or leuko-araiosis or both, and the presence of ataxic component of gait disorder most probably indicates the presence of vermian atrophy.
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PMID:Gait disorders of multi-infarct dementia. CT and clinical correlation. 847 97

We studied 34 consecutive patients with non-mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical-MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.
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PMID:The clinical and topographic spectrum of cerebellar infarcts: a clinical-magnetic resonance imaging correlation study. 849 23


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