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Three cases (case 1, female, aged 30; case 2, male, aged 32; case 3, male, aged 34) of benign brainstem encephalopathy with truncal ataxia were reported. Two patients had prodromal symptoms Neurological examination revealed truncal ataxia in all cases. As additional neurological signs, anisocoria, mydriasis, nystagmus, ptosis, transient opsoclonus, and facial palsy were seen. There was neither drowsiness nor myoclonus in the three cases. On laboratory examinations, cold agglutination test revealed significant elevation in two cases. The examination of cerebrospinal fluid showed a moderate rise of proteins in one case, but did not revealed pleocytosis in any of the cases. Magnetic resonance imaging of one patient revealed an area of high intensity in the left pontine tegmentum by T2-weighed imaging. The prognosis for all these cases was good, and the reappearance of neurological signs was not present until now. Our cases were different from brainstem encephalitis (Bickerstaff's encephalitis) because of an absence of disturbed consciousness and no pleocytosis in the cerebrospinal fluid. Our cases were also different from "myoclonus-opsoclonus syndrome" because of an absence of myoclonus. We discussed a possibility of a new clinical syndrome which we call "benign brainstem encephalopathy with truncal ataxia".
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PMID:[Benign brainstem encephalopathy with truncal ataxia--a clinical study of 3 cases]. 128 89

We describe a 40 year-old male with a ball-cage mitral valve prosthesis who suddenly developed bilateral ptosis, bilateral dilated and unreactive pupils, right third nerve palsy, bilateral failure of vertical gaze, somnolence and mild ataxia without major motor deficits. Computed Tomography (CT) revealed bilateral thalamic infarcts in the distribution of the rostral basilar artery. Infarction in this case occurred despite adequate anticoagulation. The recognition of the entity of rostral basilar artery occlusion is important as interruption of anticoagulation may be avoided.
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PMID:Nuclear third nerve palsy and somnolence due to stroke--a case report. 239 42

Groups of 25 male Sprague-Dawley rats were treated by gastric intubation with either vehicle control (modified methylcellulose) or a suspension of losulazine at 4, 8, 16, or 32 mg/kg/day for 1 yr. Ten rats/group were killed after 6 months of treatment. Reversibility of drug-induced changes was evaluated in 8 rats/group treated for 6 months and held without treatment for 5 months. Daily clinical signs and weekly body weight changes were monitored. Seminal vesicle/coagulating glands were weighed in rats treated for 6 months. Gross and microscopic evaluation of the accessory sex glands (ampullary glands, prostate, seminal vesicles and coagulating glands) was conducted in all rats killed at 6 months, after the recovery period, and in rats that survived through the one-yr treatment period. Ptosis, somnolence, and fecal softening were detected in all groups treated with losulazine. There was a nonreversible body weight gain retardation in groups treated with 8 to 32 mg/kg/day of losulazine for 6 months or 1 yr. Absolute and relative weights of the seminal vesicle/coagulating glands of treated rats were not significantly different from those of control rats. The ventral prostate in a few rats in all treated groups had yellow to tan granular foci. Treatment, but not dose-related sperm granulomas or glandular impaction with inspissated secretion (formation of corpora amylacia) in the ampullary glands, enhanced cellular exudation into the acini of the ventral prostate, and impaction of the seminal vesicles with altered granular to globular secretion were found in rats treated with losulazine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathologic changes in the accessory sex glands of rats treated with a sympatholytic hypotensive agent (losulazine). 281 27

A new patient with Leigh's syndrome (subacute necrotizing encephalomyelopathy due to pyruvate dehydrogenase complex deficiency) is presented. A Turkish boy of consanguinously married healthy parents developed progressive muscle weakness since infancy. At the age of 3 years he was unable to sit, stand or walk. Clinical examination showed general muscle weakness, hypotonia, muscle hypotrophy, bilateral ptosis, partial bilateral external ophthalmoplegia, nystagmus, intention tremor and hypoactive tendon reflexes. The EEG showed diffuse slowing, the cerebral CT scan disclosed mild hydrocephalus e vacuo. Motor nerve conduction velocity was slightly decreased, the EMG revealed signs of neuropathy. In the biopsied muscle only a mild hypotrophy of type 2 fibres was found, no abnormal mitochondria could be detected. The sural nerve was slightly abnormal: loss of large myelinated axons, loss of unmyelinated nerves. CSF protein was elevated to 80 mg/dl, protein electrophoresis revealed the pattern of markedly impaired blood-CSF barrier. Serum lactate and pyruvate were permanently elevated. In the urine the excretion of alanine was raised. The clinical state deteriorated during intercurrent infections; somnolence, vomiting and Cheyne-Stoke's respiration occurred. At the age of 3 1/2 years the child died of pneumonia. In the liver tissue a decreased activity of the pyruvate dehydrogenase complex was found. Neuropathological examination of the brain demonstrated wide-spread changes of Leigh's spongiform encephalopathy. Several enzyme deficiencies have hitherto been associated with Leigh's syndrome: This patients confirms earlier findings that a subgroup of Leigh's syndrome is caused by pyruvate dehydrogenase complex deficiency.
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PMID:[Leigh's subacute necrotizing encephalomyelopathy due to decreased activity of the pyruvate dehydrogenase complex]. 312 26

Brain-tissue shifts associated with drowsiness, stupor, and coma were studied by clinical examination and CT scanning in 24 patients with acute unilateral cerebral masses. Studies were performed soon after the appearance of the mass to detect the earliest CT changes associated with depression of consciousness. Contrary to traditional concepts, early depression of the level of alertness corresponded to distortion of the brain by horizontal displacement rather than transtentorial herniation with brain-stem compression. Horizontal displacement of the pineal body of 0 to 3 mm from the midline was associated with alertness, 3 to 4 mm with drowsiness, 6 to 8.5 mm with stupor, and 8 to 13 mm with coma. Moreover, drowsy or stuporous patients and some comatose patients had widened cisterns between the tentorial edge and the midbrain on the side of the mass, suggesting that the space was not filled by herniated medial temporal lobe. Downward displacement of the pineal body, indicating central transtentorial herniation, did not occur. Compression of one hemisphere by the other anteriorly (transfalcial herniation) was inconsistently related to alertness, though very large anterior displacements may have caused stupor in some patients. Current concepts of the pathoanatomical nature of depressed consciousness, based on pathological material obtained well after clinical examinations, may require revision, because they do not reflect early brain-tissue distortions.
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PMID:Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. 396 59

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

We describe a patient with an isolated mesencephalic dorsal tegmental infarct affecting the oculomotor nuclear complex and medial longitudinal fasciculus, documented by high-resolution computed tomography, after undergoing percutaneous transluminal coronary artery angioplasty. Clinically, the patient exhibited bilateral ptosis, bilateral internuclear ophthalmoplegia, transient convergence retractory nystagmus, and minimal somnolence. We believe the combined clinical and radiological findings favor the presence of a caudal, dorsal, and paramedian embolic infarct in the territory of the paramedian branches of the mesencephalic artery as the most likely mechanism for these exceptional findings and correlate them with Warwick's scheme of the oculomotor subnuclei.
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PMID:Oculomotor nuclear complex infarction. Clinical and radiological correlation. 647 33

Among 47 children admitted to the Chulalongkorn Medical School Hospital for neurotoxic snake bite, the attackers were identified in 15; the cobra (Naja naja) was the snake involved in all cases. Clinical manifestations in all 47 children appeared to follow a similar pattern. Drowsiness heralded the systemic effects in most of the patients. The characteristic systemic signs were those resulting from the neuromuscular effects of the venom and included ptosis, frothy saliva, slurred speech, respiratory failure, and paralysis of the skeletal muscles. These episodes occurred within 8 hours in 94% of the cases, and at the latest 19 hours following the bite. In some cases unconsciousness accompanied respiratory failure. Necrosis in the region of the bite, the prominent local sign, developed in 40% of the cases at the end of the 1st week after the bite. Infusion of specific antivenom was an effective therapeutic measure for the neuromuscular changes. Respiratory assistance was mandatory in cases of respiratory failure. Edrophonium chloride demonstrated a supportive role as a countermeasure against the neuromuscular effects.
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PMID:Clinical features of neurotoxic snake bite and response to antivenom in 47 children. 650 33

The use of sedation and monitoring in gastrointestinal endoscopy is still open for debate. In The Netherlands, generally, no systemic sedation is used for relatively simple procedures like diagnostic upper GI endoscopy and sigmoidoscopy. In most centres, for more time-consuming and burdensome endoscopies like colonoscopy, ERCP, sclerotherapy and therapeutic procedures, some form of sedation is applied. In a survey among a number of University Hospitals in The Netherlands it was shown that the sedatives mostly used are midazolam and diazepam. In more complex endoscopies these sedatives are often combined with narcotics like pethidine, morphine, fentanyl or thalamonal. Equipment to monitor the effect of these compounds on respiratory or cardiovascular function is not routinely available. However, there is a tendency towards the use of monitoring equipment and more specific to the use of pulse oximetry. Endpoints of conscious sedation are anxiolysis, amnesia and cooperation; it should not lead to ptosis, dysarthria and drowsiness. Features of drugs for conscious sedation should include these aforementioned points as well as a defined dose-effect relationship and a broad therapeutic window. Furthermore, they should be water soluble and give rapid recovery. Signs of oversedation are hypotension, bradycardia and respiratory depression. Competitive antagonists to the receptor, like flumazenil, can reverse overdosage of benzodiazepine sedatives. The sedative of choice at this moment is midazolam. When a benzodiazepine is combined with a narcotic, the narcotic should be given first and the dosage of the sedative adjusted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sedation and monitoring in gastrointestinal endoscopy. 801 67

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1. (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [loge detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [loge detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiopulmonary and behavioral responses to computer-driven infusion of detomidine in standing horses. 811 41


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