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Purpose: Visual hallucinations can occur within the central nervous system and may be associated with a lesion anywhere in the visual pathway. The purpose of this study was to assess "ictal" regional cerebral blood flow with Tc-99m ethylcysteinate dimer (ECD) SPECT in patients having acute hallucinations, and to compare the findings to the "interictal" state., Methods: A prospective study was performed to evaluate patients admitted to the neurology department with nonpsychiatric and nonepileptic visual hallucinations. The nine patients included in the study underwent thorough neurologic and psychiatric evaluations. A computed tomographic (CT) scan was performed when each patient was admitted, and electroencephalographic (EEG) recordings were made during their hallucinations. All patients underwent a brain SPECT while having acute hallucinations (ictal SPECT), and a follow-up scan was obtained 2 to 3 weeks later., Results: All patients had normal ictal EEG findings during the hallucinations. Seven of nine patients had increased perfusion on the SPECT studies in one or more regions, with a mean lesion-to-contralateral ratio of 2.1 (range, 1.5 to 2.7). Three of the seven patients had findings consistent with a cerebrovascular accident. After treatment, the hallucinations disappeared in two patients and the motor deficit improved dramatically. The follow-up SPECT study showed significant improvement in all patients 1 week later. Charles Bonnet syndrome, frontal lobe dementia, and Anton syndrome were diagnosed in three other patients, and the last one had no identifiable background disease, all with normal findings of EEG, CT, and magnetic resonance examinations. They all responded readily to carbamazepine therapy, and the follow-up SPECT study showed resolution of the findings. Two of nine patients showed posterior cortical hypoperfusion, and eventually Lewy body disease was diagnosed. The SPECT showed no evidence of regional hyperperfusion., Conclusions: This prospective preliminary study suggests that brain imaging using SPECT may be useful in identifying the mechanisms and evolution of blood flow abnormalities in certain subgroups of patients who have visual hallucinations and may assist in the selection of specific therapy.

Background: Transcranial Doppler is a sensitive instrument for the diagnosis of brain death. The guidelines for the determination of brain death include the demonstration of specific blood flow patterns in the anterior and posterior circulation systems. A limitation of this method is the frequent false finding of no flow, especially when using the transtemporal approach in older women., Objective: To evaluate the efficacy of the transorbital approach in the diagnosis of brain death using transcranial Doppler., Methods: A prospective controlled, diagnostic test study was performed. Transorbital, transtemporal, and transforaminal approaches were used. Fifty-seven patients (29 men and 28 women; mean +/- SD age, 68.2 +/- 12.1 years) with clinically determined brain death were examined., Results: In 45 patients, oscillatory flow or systolic spikes were found in all approaches. In 4 patients, no flow was detected. In 6 patients, oscillatory flow or systolic spikes were found in 2 approaches, including the transorbital one. In 2 patients, a positive finding was demonstrated only using the transorbital approach. Using the transorbital approach, the percentage of positive findings with definitive diagnoses of brain death rose from 79% to 88%., Conclusion: The transorbital approach is a useful addition for the diagnosis of brain death, using the transcranial Doppler technique.

The Mollicutes (Mycoplasma, Acholeplasma, and Spiroplasma) are the smallest, simplest and most primitive free-living and self-replicating known cells. These bacteria have evolved from Clostridia by regressive evolution and genome reduction to the range of 5.8 x 10(5)-2.2 x 10(6) basepairs (bp). Structurally, the Mollicutes completely lack cell walls and are enveloped by only a cholesterol containing cell membrane. The Mollicutes contain what can be defined as a bacterial cytoskeleton. The Spiroplasmas are unique in having a well-defined, dynamic, helical cell geometry and a flat, monolayered, membrane-bound cytoskeleton, which follows, intracellularly, the shortest helical line on the cellular coil. By applying cryo-electron-microscopy to whole cells, isolated cytoskeletons and cytoskeletal fibrils and subunits, as well as by selective extraction of cellular components, we determined, at a resolution of approximately 25 A, the cellular and molecular organization of the cytoskeleton. The cytoskeleton is assembled from a 59 kDa protein. The 59 kDa protein, has an equivalent sphere diameter of approximately 50 A. Given the approximately 100 A axial and lateral spacings in the cytoskeletal ribbons and the near-circular shape of the subunit, we suggest that the subunit is a tetramer of 59 kDa monomers; the tetramers assemble further into flat fibrils, seven of which form a flat, monolayered, well-ordered ribbon. The cytoskeleton may function as a linear motor by differential and coordinated length-changes of the fibrils driven by conformational changes of the tetrameric subunits, the shape of which changes from near circular to elliptical. The cytoskeleton controls both the dynamic helical shape and the consequent motility of the cell. A stable cluster of proteins co-purifies with the cytoskeleton. These apparent membrane and membrane-associated proteins may function as anchor proteins.

Sixty-five adult patients who had acute peripheral vestibulopathy (APV) were followed-up to determine their functional outcome. During the acute phase, they were treated with betahistine and mobilization. In the entire study population, APV was not significantly associated with a change in occupational activities, physical work or driving ability. Older individuals had significantly attributed a change in work to disease other than APV. Change attributed to APV occurred significantly more frequently in women than in men. The therapeutic approach seems beneficial.

A randomized, placebo-controlled, double-blind study was performed as a pilot study to examine the benefit of the administration of magnesium sulfate given intravenously as a protective substance during the first 24 hours following a stroke. Patients who had cortical infarction in the middle cerebral artery territory with moderate to severe neurologic deficits lasting for more than 15 minutes with onset less than 24 hours were included. The patients were treated with magnesium sulfate or placebo for 5 days and examined by a blinded investigator. Patients had follow-up for 30 days. The primary efficacy variable was the proportion of patients reaching mild to moderate neurologic deficit on the Orgogozo scale (80 points) and relative functional independence on the Barthel index (60 points). Orgogozo scale and Mathew scale values were obtained on admission and days 2, 4, 8, and 30 after stroke. Barthel activities of daily living index and Rankin disability score were obtained on day 30. Forty-one patients (22 given treatment and 19 given placebo) demonstrated significant beneficial effects on the Orgogozo scale (84 +/- 11 vs. 64 +/- 10, p < 0.0001) and (83 +/- 14 vs. 70 +/- 15, p < 0.009), respectively. At the end of 1-month follow-up, the Barthel ADL index was nonsignificantly higher and the Rankin disability score was marginally significantly lower in the magnesium-treated group (84 +/- 26 vs. 71.8 +/- 26, p < 0.143) than in control subjects (2.3 +/- 1.1 vs. 3 +/- 1.3, p < 0.077). Intravenous magnesium sulfate had significant positive effect on the outcome in patients with acute stroke. Further studies on a larger scale are needed to confirm these findings.

Early seizures caused by stroke are a common cause of epilepsy in adults. The protocol for treatment in such a case is not clear. Patients were studied retrospectively after early poststroke seizures. Two groups of patients were compared: one treated group included 35 patients who continued therapy for 2 years; the second group of 23 patients were untreated following a first attack, receiving anticonvulsive therapy only after a second seizure. The data of 61 patients (35 treated and 26 untreated) were analyzed. In the treated group, 24 patients were on treatment with carbamazepine, 9 with valproic acid and 2 with phenytoin. Seizure-free rate after 2 years was 85% in group I and 61% in group II (p = 0.042). Comparing the seizure rate and the event-free period (number/follow-up at risk) during the 2 years of no anticonvulsive therapy, both groups experienced about the same seizure rate (4.8 vs. 6.2%, p = 0.605) and similar seizure-free curve survival analysis (p = 0.85). We conclude that treatment of seizures immediately after the first attack after cerebral infarctions decreases the risk of recurrent seizure during the first 2 years of antiepileptic treatment. This subgroup of patients receiving antiepileptic medication immediately after the first poststroke seizure continues to be at the same rate of risk after treatment was stopped as the untreated group during the first 2 years. Antiepileptic therapy is an option in the medical management of poststroke seizure patients, but has no influence on the development of recurrent seizures after discontinuing medication., (Copyright 2001 S. Karger AG, Basel)

Distal limb weakness is an uncommon manifestation of myasthenia gravis and has rarely been reported. We report on a patient whose sole manifestation of myasthenia gravis was dorsiflexor weakness for 6 months. Bilateral foot drop, although rare, should be considered in the differential diagnosis of myasthenia gravis.

Rhabdomyolysis is described as an adverse event of simvastatin therapy either by itself or in combination with other medications. It is unclear whether this phenomenon is specific to simvastatin or to all cholesterol-lowering agents as single-dose therapy or caused by the association of special coadministered medications. We describe two cases in which rhabdomyolysis developed after coadministration of simvastatin (20 mg/d) and the antifungal ketoconazole. The clinical features, blood examination results, and positive outcome were very similar in both cases. We concluded that ketoconazole, an antifungal sterol synthetic inhibitor of the azol group, may induce rhabdomyolysis in patients undergoing treatment with simvastatin, a lipid lowering agent, and increase the possibility of muscle-damaging adverse events of the agents.

Magnesium has been reported to have a dilatatory effect on cerebral arteries. Reduction of extracellular Mg+2 has been shown to be directly correlated with the intensity of cerebral spasm. A neuroprotective effect of magnesium in stroke has also been hypothesized. The aim of our study was to examine the Mg+2 levels in serum and cerebrospinal fluid (CSF) in the early stage of stroke and to evaluate the correlation between Mg+2 levels and the development of neurological deficits. Between 1986 and 1994, 96 patients who had a stroke of 24- to 48-h duration were enrolled in the study. Serum and CSF levels of magnesium were checked on admission, 2448 h after the onset of stroke. Using a neurological score, the neurological deficit was assessed on the 1st day, 1 and 4 weeks later. Computed tomography (CT) was performed after 1 week, and the volume and location of infarction were calculated and measured. Statistical analysis was performed for cortical and subcortical patients separately, using Spearman correlation and multiple linear and logistic regression analyses. Significant correlation was found between CSF Mg+2 and the size of the infarct (P < 0.0001). There was no correlation between serum Mg+2 and CSF Mg+2 levels. Regression analysis demonstrated an increase in the values of the Mathew Neurological Score with higher CSF Mg+2 levels. This association remained true after other factors such as age, associated heart disease, diabetes and infarction size had been taken into account by the regression model. The results confirm that there is a relationship between a low Mg+2 concentration in CSF during the first 48 h after onset of ischaemic stroke and the intensity of the neurological deficit. The therapeutic consequence of this finding may have some importance.

Background and Purpose: Endothelin 1 (ET-1), a highly potent endogenous vasoactive peptide, exerts a sustained vasoconstrictive effect on cerebral vessels. Elevation of ET-1 in plasma has been reported 1 to 3 days after ischemic stroke. Since we assumed that a much faster and more intense response may be observed in the cerebrospinal fluid (CSF) and since an increase in concentration of ET-1 in the CSF may cause constriction of cerebral vessels and eventually influence the neurological outcome, we measured ET-1 values in the CSF within 18 hours of stroke onset and compared the values with those in the plasma., Methods: Twenty-six consecutive patients with acute stroke were clinically evaluated according to the modified Matthew Scale and underwent two repeat CT scans. Within 5 to 18 hours of stroke onset, lumbar puncture and blood samples were concomitantly obtained and tested; ET-1 levels in CSF and plasma of these patients were analyzed by radioimmunoassay and compared with the levels of a control group of patients with no neurological disease., Results: The mean CSF concentration of ET-1 in the CSF of stroke patients was 16.06 +/- 4.9 pg/mL, compared with 5.51 +/- 1.47 pg/mL in the control group (P < .001). It was significantly higher in cortical infarcts (mean, 17.7 +/- 4.1 pg/mL) than in subcortical lesions (mean, 10.77 +/- 4.1 pg/mL) (P < .001) and significantly correlated with the volume of the lesion (P = .003). The correlation between ET-1 levels in the CSF and the Matthew Scale score was less significant (P = .05). Plasma ET-1 level was not elevated in any group., Conclusions: ET-1 is found to be significantly elevated in the CSF of stroke patients during the 18 hours after stroke. No elevation was demonstrated in plasma at this time period. ET-1 may be used as an additional indicator of ischemic vascular events in the early diagnosis of stroke. The dissimilarity between the CSF and plasma ET-1 concentrations may lead also to an hypothesis that there is a vasoconstrictive effect on the cerebral vessels or a neuronal effect caused by ET-1 in the mechanism of the progression of brain ischemia.

Unlabelled: The aim of this case report was to present a patient with complete anarthria and orofacial apraxia without other relevant neurological deficit. The clinical features are compatible with anterior operculum syndrome., Methods: A regional brain perfusion scan was done using 99mTc-HMPAO and a SPECT gamma camera. A brain CT scan and an MRI were also performed., Results: Brain CT and MRI were not diagnostic. On brain SPECT, hypoperfusion of the left inferior area of the frontal lobe was noted., Conclusion: The patient studied showed an uncommon case of anterior operculum syndrome of focal degenerative origin localized by SPECT. SPECT may be a useful and effective method for diagnosis of this unusual neurological deficit.

Thyroid function was examined periodically in a group of 85 patients treated with low-dose amiodarone, and followed for 1-13 years (mean 3.6). Biochemical hypothyroidism (elevated thyroid stimulating hormone (TSH) only) developed in 8 patients and clinical hypothyroidism in 3, while hypothyroidism developed in 5. In the first 11 cases amiodarone was continued but 1-thyroxine was added. In the 5 that became hyperthyroid, amiodarone was stopped and thyroid function became normal within a few months. In the 69 patients without thyroid dysfunction, elevated thyroxine (T4) and free thyroxine index (FTI) were found in 20% and 17%, respectively, and elevated free T4 (FT4) in 28%; all had normal total tri-iodothyronine (TT3) and TSH. In practically all patients, reverse T3 (rT3) rose more than 30% above initial levels. It is concluded that in patients treated with low dose amiodarone: 1) thyroid function should be followed closely; 2) elevated levels of TT4, FTI and FT4 do not necessarily imply hyperthyroidism; 3) hypothyroidism may be biochemical only, without progression to overt hypothyroidism, despite continued treatment; 4) both the hypo- and the hyperthyroidism induced are usually reversible; 5) amiodarone may be continued despite onset of hypothyroidism, provided replacement therapy is given.

Complications of low-dose amiodarone in 83 patients, in whom the drug was effective and who were followed for 1-13 years, are presented. Hypothyroidism was diagnosed in 11 (in 8 by the finding of elevated TSH). In 2 of the 3 in whom clinical signs of hypothyroidism were evident, amiodarone was continued, but thyroxine was also given. In 5 others thyrotoxicosis ensued. Propylthiouracil (PTU) was given and amiodarone was discontinued. PTU was then stopped within 4-8 months, without recurrence of the hyperthyroidism. In 1 patient pneumonitis resolved spontaneously a few weeks after stopping amiodarone. Because of gastrointestinal distress amiodarone was stopped in 1 patient. In none were liver enzymes elevated, nor was the nervous system affected clinically. Photosensitivity in 6 patients and skin discoloration in 2 did not necessitate discontinuation of the drug. Blurred vision was reported by 4, but its connection with amiodarone was not proven. There was sinus bradycardia in 2. There was no arrhythmic effect of amiodarone seen on ECG nor on Holter monitoring, nor was there any mortality. We conclude that amiodarone in low doses causes many complications, most of them mild and transient. However, in only a few cases is discontinuation of the drug indicated.

Five adult patients were admitted to the neurological department in a state of status epilepticus. All were treated unsuccessfully with IV diazepam and diphenylhydantoin. Administration of sodium valporate or phenobarbital also was ineffective. However, after treatment with intrarectal chloral hydrate, all seizures ceased. The excellent effect of this drug was proved both clinically and electrodiagnostically. Discussed is the possibility of using chloral hydrate to treat patients with status epilepticus in whom conventional treatment has failed.

Remote metastases, leptomeningeal dissemination and spreading of the tumor by infiltration are rare complications of glioblastoma multiforme. The existence of different forms of spreading simultaneously is very rare. We present a case of a young patient with glioblastoma multiforme who was operated and subsequently received radiation therapy and cytotoxic treatment. Eight months following the operation, the patient developed cauda equina syndrome. Bone metastases of vertebrae and ribs, and direct infiltration of the recurrent tumor mass into the ethmoidal and frontal sinuses were found. The described patient demonstrates a very rare combination of all forms of spreading metastases in glioblastoma multiforme. The infiltration of the tumor mass into the sinuses and the direct permeation of the meningeal and dural venous system and of the leptomeninges, may explain the mechanism of the development of distant metastases and leptomeningeal dissemination in glioblastoma multiforme.