bluuebunny/crossref_metadata_2025 huggingface dataset:
Mianserin, a 5‐HT2receptor antagonist, in the treatment of delirium: an open study
Authors: Ikeguchi K. , Kuroda A.
Published: January 2011

To determine the role of the serotonin system at the 5‐HT2receptors on delirium in the aged, we assessed the effects of mianserin, a relatively selective 5‐HT2receptor antagonist, in such patients. Twenty‐six delirious patients [four without dementia, nine with Alzheimer's disease (AD), 13 with ischemic vascular dementia (IVD)] were included in the open study. After the dose titration period, the mean dose of mianserin administrated was 31.2 mg in delirious patients without dementia, 25.0 mg in delirious patient with AD and 25.9 mg in delirious patients with IVD. The average total score of each patient group on a symptom rating scale was reduced significantly within 24 h (p< 0.05). A complete elimination of symptoms was noted in all four delirious patients without dementia. In the nine delirious patients with AD, marked improvement was noted in four patients (44.4%), moderate improvement in four (44.4%) and no improvement in one (11.1%). In the 13 delirious patients with IVD marked improvement was noted in seven (53.8%), moderate improvement in five (38.5%) and no improvement in one (7.7%). The rapidity of the improvement may be attributable to mianserin's antagonism at the 5‐HT2receptors, and such serotonin antagonism at the 5‐HT2receptors may be important in treating delirium.‐
5‐HT1receptors in migraine pathophysiology and treatment
Authors: Ferrari M.D. , Saxena P.R.
Published: January 2011

Migraine is a frequent paroxysmal headache disorder of unknown aetiology. Genetic factors may control attack frequency and possibly attack severity. Serotonin1D(5‐HT1Dβ) receptors have a prominent position within the final common pathway of the mechanisms involved in the headache and associated symptoms. Stimulation of these receptors by selective 5‐HT1Dβreceptor agonists such as sumatriptan and newer compounds including MK‐462 and 311C90, rapidly and fully blocks the symptoms of the headache phase. The efficacy depends on factors such as timing of administration during or before the headache, speed of initial rise of drug plasma levels, and possibly degree of brain penetration. All agonists at S‐HT1Dβreceptors share a short duration of action resulting in recurrence of the headache symptoms within 24 h in about one‐third of attacks in clinical trials. The risk for headache recurrence seems patient dependent: about 10% of patients treating multiple attacks experience headache recurrence in every treated attack, whereas 40% never experience recurrence. These differences are not related to simple pharmacokinetic differences between patients or drugs. Increasing plasma half‐life of the drug will most likely not reduce the risk of recurrence. “Breakthrough of peripheral suppressive effect” with an ongoing “central migraine generator”, rather than the occurrence of a new attack, seems to be the most likely underlying mechanism for headache recurrence. In a minority of, possibly predisposed, patients, use of sumatriptan may induce increase of attack frequency. Four mechanisms have been suggested for the antimigraine action of 5‐HT1Dβreceptor agonists: (1) vasoconstriction of cranial, most likely meningeal and dural blood vessels; (2) inhibition of release of vasoactive neuropeptides from perivascular trigeminal nerve terminals within dura mater and meninges; (3) blockade of trigeminal nerve terminal depolarization; and (4) central inhibition within the trigeminal nucleus caudatus in the brainstem. Which of these mechanisms is the most important, and whether or not vasoconstrictor action is necessary for antimigraine efficacy, is currently under extensive investigation. At this point all drugs with proven antimigraine efficacy share the ability to contract blood vessels and thus all feature also the potential risk of causing vasoconstriction of coronary vessels. In relation herewith, major efforts are put into the search for “the antimigraine receptor” and which receptor subtype mediates which action of sumatriptan‐like drugs. At this point, the 5‐HT1Dβreceptor subtype is thought to mediate vasoconstriction. Some investigators feel that the 5‐HT1Dαreceptor subtype mediates the neuronal effects of sumatriptan, while others are much less convinced about the physiological role of this subtype of receptor. Further research into receptor subtype specificity and affinity of compounds may promote the development of even better antimigraine drugs.
Decreased CSF levels of homovanillic acid in ALS patients
Authors: Testa D. , Colangelo A.M. , Fetoni V. , Parati E.
Published: January 2011

Levels of homovanillic acid (MVA) were measured in lumbar cerebrospinal fluid from 24 patients affected by amyotrophic lateral sclerosis (ALS) and compared with those found in 11 patients with Parkinson's disease (PD) and 10 patients with lumbar disc herniations who served as controls. Mean HVA levels were significantly decreased in ALS and PD patients. These findings are consistent with impairment of central dopaminergic systems in ALS as well as suggesting degeneration of neuroanatomical structures other than motor neurons.
Isoflurane for 7 days in refractory status epilepticus
Authors: Hilz M. J. , Erbguth F. , Stefan H. , Neundörfer B.
Published: January 2011

There is limited experience with continuous (>3 days) isoflurane anesthesia for status epilepticus (SE). We present a case with prolonged SE, probably due to thallium intoxication, in which isoflurane successfully suppressed seizure activity over 7 days without adverse effects. When isoflurane was discontinued, seizures returned despite high doses of barbiturates, and the patient died several months later. Early isoflurane anesthesia is an effective alternative therapy in prolonged convulsive SE resistant to common therapy and intravenous general anesthesia. However, its continuous application for several days requires familiarity with anesthesiologic principles, and scavenging of expiratory air.
Potentiation instead of habituation characterizes visual evoked potentials in migraine patients between attacks
Authors: Schoenen J. , Wang W. , Albert A. , Delwaide P.J.
Published: January 2011

We have studied habituation of the pattern‐reversal visual evoked potential (VEP) in healthy volunteers (n= 16) and in patients suffering from migraine without (n= 27) or with aura (n= 9). Five blocks of 50 responses at a stimulation rate of 3.1 Hz were sequentially averaged and analyzed separately for latencies, peak‐to‐peak amplitudes of N1‐P1 and P1‐N2, and the area under the N2 component Latencies of N1, P1, or N2 components were not significantly different between the sequential trial blocks, or between groups. Mean amplitudes of N1‐P1 and P1‐N2 in the first and subsequent blocks of SO responses were not statistically different among groups. In healthy subjects, there was a decrement of N1‐P1 and P1‐N2 amplitudes and N2 area on successive averagings. This habituation was maximal in the third and fourth blocks, but tended to disappear in the fifth block. In marked contrast to healthy subjects, migraine patients were characterized by a transient amplitude increment (i.e. potentiation) of VEP components which reached its maximum in the second to fourth blocks. Amplitude changes in sequential blocks were not dependent on attention and differed significantly between healthy subjects and migraineurs, but not between migraine with and without aura. Taken together with previous studies showing deficient habituation of contingent negative variation in migraine, these results indicate a dysfunction of central information processing which might have behavioral and pathogenic correlates.
Efficacy of antibiotics in neurobrucellosis
Authors: AbdulJabbar M.
Published: January 2011

Brucellosis is a systemic infection that rarely involves the nervous system. This paper describes 21 cases of neurobrucellosis affecting different parts of the peripheral and central nervous system. The various presentations closely simulated acute meningoencephalitis, myelitis, cerebral ischaemia, radiculopathy or multisystem degeneration. All patients received adequate combined antimicrobial therapy of trimethroprim‐sulfamethoxazole, doxycycline, and/or rifampicin. The improvement was quick and complete in meningoencephalitic patients, while others with structural changes in the nervous system did not recover and ended up with permanent deficits. The combination regimen and duration of therapy are the focus of this study.
Evoked potentials in mitochondrial disorders
Authors: Muñoz‐Málaga A. , Boza F. , Blanco A. , Bautista J.
Published: January 2011

Twenty‐eight adult patients with mitochondrial disease were evaluated with muitimodal evoked potentials (EPs) to assess a possible CNS involvement The patients were classified into five groups: encephalopathy (two cases), progressive external ophthalmoplegia (PEO; four cases), pure myopatby (15 cases), cardiomyopathy (five cases) and asymptomatic relatives (two cases). EPs showed differences between encephalopathy (all EP modalities affected) and PEO groups (all patients with at least one EP altered), with lesser degrees of affection in pure myopathy and cardiomyopathy groups. The asymptomatics registered normal EPs. In view of these results, progressive CNS damage in mitochondriopathies, expressed by abnormal EPs, can be established as follows (from greatest to minor severity): encephalopathy, PEO, pure myopathy/cardiomyopathy and asymptomatic condition.
Central defects of autonomic function in secondary progressive multiple sclerosis: observations based on cardiovascular and growth hormone responses to clonidine
Authors: Thomaides T.N. , Zoukos Y. , Chaudhuri K. Ray , Watson L. , Mathias C.J.
Published: January 2011

The haemodynamic, autonomic and hormonal effects of the centrally acting sympatholytic drug clonidine have been studied in 10 patients with secondary progressive multiple sclerosis (MS) and 10 age‐ and sex‐matched normal subjects (controls). Detailed physiological studies, previously described in these 10 MS patients, indicated that none had postural hypotension or an abnormal Valsalva manoeuvre; six, however, had impaired responses to a range of pressor tests, suggestive of a central autonomic abnormality. In the controls after clonidine, there was a fall in blood pressure and superior mesenteric artery vascular resistance. Finger temperature and growth hormone levels rose. In the MS patients after clonidine, the haemodynamic responses varied. In five out of ten MS patients, as in the controls, there was a fall in blood pressure and superior mesenteric vascular resistance, while finger temperature rose. There was no haemodynamic response to clonidine in the other five MS patients. In eight out of ten MS patients there was no rise in plasma growth hormone levels after clonidine. The abnormal haemodynamic responses to clonidine, taken in conjunction with the previous physiological studies, suggest involvement of central sympathetic interconnections in five of the MS patients, probably as part of the demyelinating process. The impaired growth hormone response to clonidine occurred in a greater number of patients and may indicate lesions in the hypothalamus. These observations in MS patients, without overt clinical evidence of autonomic failure, indicate that the haemodynamic and growth hormone responses to clonidine may be an early indicator of autonomic dysfunction involving central autonomic centres and pathways.
Acute posterior multifocal placoid pigment epitheliopathy presenting as an aseptic meningitis
Authors: Manto M. , Cordonnier M. , Blecic S. , Legros B. , Hildebrand J.
Published: January 2011

We report a 33‐year‐old patient with acute posterior multifocal placoid pigment epitheliopathy presenting as steroid‐responsive aseptic meningitis. Four unusual biological abnormalities were present: an elevated erythrocyte sedimentation rate, circulating immunocomplexes, an oligoclonal banding in cerebrospinal fluid and a transient abnormal urine sediment All these and the prompt response to corticosteroids give support to the hypothesis of a systemic autoimmune disease.
Huntington's disease: a multidisciplinary study
Authors: Ruiz P.J. Garcia , Del Barrio A. , Barroso T. , Tortosa E. Gómez , Benitez J. , Astarloa R. , De Yébenes J. Garcia
Published: January 2011

Huntington's disease (HD) is characterized by the presence of movement disorders, cognitive decline and psychiatric disturbances. Recently, the gene responsible for HD has been found. As a result, a more direct test for HD is available. This may lead to a comprehensive approach to HD, since it is now possible to study HD patients without uncertainties in diagnosis. We carried out a clinical‐genetic study on 45 patients with HD. We performed molecular analysis on 39 patients. All had an abnormal expansion of (CAG)n ranging from 41 to 90 triplets (mean 50.8 ± 11.5 S.D.). There was a strong inverse correlation between (CAG)n expansion and age at onset Gender of the affected parent influenced age at onset (p < 0.001) and number of triplets (p < 0.001). A significant impairment of akinesia (p < 0.001), chorea (p < 0.005), MMSE (p < 0.01) and Rey scores (p < 0.05) occurred across successive stages of functional disability. Hooper Visual Organization Test (HVOT) scores did not change significantly across stages, but this test was extremely useful to discriminate between patients at an early stage and controls. A significant correlation was found between functional disability and motor‐cognitive decline; correlation was stronger for motor (akinesia, r = 0.77; chorea, r = 0.61) than for cognitive aspects (MMSE, r = ‐ 0.54; Rey, r = ‐ 0.51; HVOT, r = ‐0.35).
Apolipoprotein E allelic variants predict dementia in elderly patients with memory impairment
Authors: Coria F. , Rubio I. , Bayón C. , Cuadrado N. , Santaengracia N. , Rodriguez‐Artalejo F.
Published: January 2011

Apolipoprotein E‐ɛ4 (ApoEɛ4 allele is a major risk factor of late‐onset Alzheimer's disease (AD). We now report that: (1) this allelic variant is more frequent among patients with age‐associated memory impairment (AAMI) than among healthy control subjects; (2) after a 3 year follow‐up, those AAMI patients who developed dementia had ApoEɛ4 more frequently than those who did not; (3) ApoE allele distribution did not differ significantly between demented AAMI and late‐onset AD patients. These results suggest that ApoEɛ4 predicts the development of dementia in AAMI patients, and that AAMI, an idiopathic amnesic syndrome of high prevalence among the elderly, and late‐onset AD are different stages of the same disorder.
Invasion of a subcutaneous Aspergillus abscess into the brain
Authors: Vandenberghe R. , Marchau M.
Published: January 2011

We present the case of a 57 year old woman with contiguous infection by Aspergillus fumigatus. The lesion started subcutaneously, forming an abscess. Seventeen days later we observed an intracranial abscess, infection of the frontal sinus and destruction of the frontal bone between the subcutaneous abscess and the sinus.
Serum levels of nitrates in focal cerebral ischemia
Authors: Molina José Antonio , Jiménez‐Jiménez Félix Javier , Navarro José Antonio , Ruiz Eduardo , Arenas Joaquin , Pérez‐Sempere Angel , Egido José Antonio , Soriano‐Soriano Cristina , Ayuso‐Peralta Lucia , Fernández‐Calle Pilar
Published: January 2011

To ascertain the possible role of nitric oxide (NO) as risk factor for cerebral ischemia, we studied the serum levels of nitrate (oxidation product that provides an indirect estimation of NO), in 49 patients between the 3rd and 7th days after a cerebral ischemic event (TIAs, RIND and cerebral infarction) and in 65 matched controls. The serum levels of nitrate did not differ significantly between cerebral ischemic patient and control groups (42.6 ± 334 and 44.8 ± 2.67 ± μmol/l, respectively). They were not influenced by age, blood pressure, or smoking and alcohol‐drinking habits. These results suggest that serum levels of nitrate are apparently unrelated to the risk for cerebral ischemia.
A double‐blind, placebo‐controlled, enriched population study of tacrine in patients with Alzheimer's disease
Authors: Forette F. , Hoover T. , Gracon S. , de Rotrou J. , Hervy M.P. , Lechevalier B. , Micas M. , Petit H. , Orgogozo J.M. , Guard O. , Saudeau D. , Forette B. , Michel B. , Emile J. , Augustin P. , Wang A. , Vignat J. , Allain H. , Cuny G. , Leger J. M. , Collard M. , Joyeux O. , Khalil R.
Published: January 2011

The efficacy of tacrine in the treatment of patients with probable Alzheimer's disease (AD) was evaluated in a double‐blind, placebo‐controlled, enriched population multicenter study in France. A total of 280 patients entered the dose titration phase of the study. The assessment of potential benefit of tacrine (“best dose”) was based on demonstrating improvement on the Alzheimer's Disease Assessment Scale (ADAS) total score versus a blinded placebo. One hundred and thirty of 242 (54%) patients achieved a “best dose” and were eligible for the double‐blind, parallel group (pivotal) phase. Primary efficacy measures were ADAS‐Cognitive and Clinical Global Impression of Change; secondary efficacy measures of cognition and activities of daily living were also included. Results indicated that tacrine‐treated patients showed improved functioning based on the ADAS‐Cognitive in comparison to placebo‐treated patients. Transaminase elevations above the upper limit of normal occurred in 32% of patients, were more frequent in women than in men, demonstrated a delayed onset, and returned to normal limits for all patients following discontinuation of treatment The results from this study are supportive of the efficacy of tacrine in the treatment of AD as demonstrated in a study of similar design conducted in the US and studies using different designs.
Progressive supranuclear palsy: clinical and pathological diagnosis
Authors: Tolosa E. , Valldeoriola F. , Cruz‐Sánchez F.
Published: January 2011

Progressive supranuclear palsy (PSP) is an heterogeneous disorder, both clinically and pathologically and, in consequence, it is often difficult to diagnose. In this review we shall discuss those clinical settings in which it is difficult to make the diagnosis of PSP and review the pathology of the disorder. Clinical and pathological diagnostic criteria currently in use will also be discussed.
Persistent increase of leukocyte aggregation in a patient with relapsing ischemic stroke and ulcerative colitis
Authors: Silvestrini M. , Pietroiusti A. , Matteis M. , Magrini A. , Bernardi G. , Galante A.
Published: January 2011

There is an increased incidence of central nervous system thromboembolic events in patients with inflammatory bowel disease. The possible pathogenetic link between the two diseases is not clear. Experimental and clinical observations suggest the possible role of leukocyte activation in the induction of ischemic and inflammatory events. In a patient with relapsing ischemic stroke and ulcerative colitis, serial determinations of leukocyte aggregation, by means of the modified leukergy test, were performed. A persistent increase of the percentage of aggregated leukocytes with values much higher than those of healthy subjects and patients with ischemic stroke was found during and between the episodes of ischemia and inflammation. The particular temporal pattern of clinical and hemorheological alterations suggests that the persistent activation of leukocytes may represent a risk factor for the development of both ischemic and inflammatory disease.
Entacapone in combination with standard or controlled‐release levodopa/carbidopa: a clinical and pharmacokinetic study in patients with Parkinson's disease
Authors: Kaakkola S. , Teräväinen H. , Ahtila S. , Karlsson M. , Naukkarinen T. , Rita H. , Gordin A.
Published: January 2011

We investigated clinical response and pharmacokinetics of levodopa when entacapone, a catechol O‐methyltransferase (COMT) inhibitor, was administered concomitantly with either a standard (Std) or a controlled‐release (CR) levodopa/carbidopa preparation to 12 patients with Parkinson's disease. An open cross‐over study consisted of the initial study day without entacapone followed by two 10‐day treatment periods with a study day at the end of each period. The patients who received entacapone (200 mg t.i.d. or q.i.d.) concomitantly with Std levodopa/carbidopa (200/50 mg t.i.d. or q.i.d.) during the first period received subsequently entacapone with CR levodopa/carbidopa (200/50 mg t.i.d. or q.i.d.), and vice versa. On the study days, the patients took the medication at 8 a.m. and the second dose 6 h later. We evaluated the disability before drug administration and then 1‐h intervals for 8 h. Repeated blood samples were taken for analysis of plasma levodopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), carbidopa, and entacapone. Entacapone decreased significantly the clinical disability with both Std and CR levodopa, slightly more with Std levodopa. The clinical response started earlier with Std levodopa whereas the “on”‐time increased by about 1 h, equally with both levodopa preparations. Std levodopa produced 23% higher area under the curve (AUC) of levodopa than the CR preparation, but entacapone increased the AUC approximately equally, 33% with Std and 36% with CR levodopa. Entacapone slightly decreased Cmax of levodopa in combination with Std levodopa, whereas it increased that with CR levodopa. The AUC of 3‐OMD was about 20% smaller after Std than after CR levodopa. Entacapone decreased the AUC of 3‐OMD by 38–40% with both levodopa preparations. Entacapone did not modify the AUC levels of carbidopa although its bioavailability was less from CR levodopa than from Std levodopa. In three patients levodopa dosage was reduced when on Std levodopa because of nausea. Otherwise, the treatments were well tolerated. The study shows that entacapone is an effective COMT inhibitor when combined with either Std levodopa or CR levodopa.
Interleukin‐2, its soluble receptor, and soluble T8 antigen in acute ischemic stroke
Authors: Grau A.J. , Mathias D. , Banerjee T. , Hacke W.
Published: January 2011

The treatment of neoplasia with interleukin‐2 (IL‐2) can be complicated by neurological deficits resembling transient Ischemic attack and stroke. We investigated whether interleukin‐2 contributes to the natural course of cerebrovascular ischemia and particularly to the pathogenesis of infection‐associated stroke. Plasma levels of interleukin‐2 were below the level of detectability in almost all measurements. Patients with and without previous infection (n = 11, 805 ±445 U/ml vs n = 19, 824 ± 501 U/ml) did not have significantly higher levels of soluble interleukin‐2 receptors than control subjects with (n = 14, 667 ± 229 U/ml) or without vascular risk factors (n = 17, 567 ± 176 U/ml). Receptor levels increased in patients during the first week after stroke (n = 15, 1157 ± 1013, p < 0.02). Levels of soluble T8 antigen (sT8) were higher in patients (n – 26, 320 ± 112 U/ml) than in healthy control subjects (n = 15, 246 ± 92 U/ml; p < 0.05) and sT8 levels increased during the first week after stroke (p < 0.05). These results reflect an immunological response to the cerebral infarct; they do not indicate a general role of the IL‐2 system in the pathogenesis of ischemic stroke with or without previous infection.
Arterial mechanisms in the pathophysiology of migraine headache—implications for modern therapy
Authors: Thomsen L.L.
Published: January 2011

Studies of the cephalic vascular system have markedly contributed towards an understanding of the mechanisms of migraine pain. Whereas cerebral blood flow changes, and thereby changes in the arterioles, correlate poorly with migraine headache, abnormal regulation of the large cranial arteries seems to play a significant role in relation to migraine pain. Thus, vasodilation of extra‐ and intracranial conductance arteries has been described both during spontaneous migraine attacks and during experimentally provoked vascular headaches. Whether dilation of these arteries is the key mechanism of migraine nociception or is merely associated with another more important nociceptive mechanism remains to be shown. Studies of vascular regulatory mechanisms have not only pointed towards a possible locus of migraine pain, but have also been helpful in demonstrating a new molecular mechanism of migraine—the key effect of the small messenger molecule nitric oxide. It is likely that nitric oxide is the most important molecule responsible for the induction of migraine attacks.
Molecular biology and genetics of Alzheimer's disease
Authors: Jiménez‐Escrig A. , Bianco‐Jerez C. , Orensanz LM.
Published: January 2011

The recent progress in molecular biology research has changed the past concepts on Alzheimer's disease (AD) and other nervous system amyloidoses. This paper compiles the basic principles of molecular biology of AD and reviews their clinical impact The new data about the function and metabolism of amyloid precursor protein and the more recent information on the role of the apolipoprotein E have provided new insight into the pathogenesis of this disease. Although further investigations are still required to assemble these data into a theory that completely explains the development of the disease and changes the present symptomatic therapeutic strategies to an entire preventive or curative approach, the recent research results in this field are relevant for the diagnostic and therapeutic management of AD patients.
A Japanese family with Machado‐Joseph disease characterized by initial emaciation and myoclonus
Authors: Aoki M. , Abe K. , Nagata T. , Kameya T. , Watanabe M. , Onodera H. , Mochizuki H. , Itoyama Y.
Published: January 2011

We describe a Japanese family with hereditary spinocerebellar ataxia characterized by initial emaciation and myoclonus. The proband first noted truncal ataxia, myoclonus in the shoulder and general emaciation at age 24. The other affected members of the family also had such emaciation in the early stage of the disease. The DNA analyses of the family revealed that the patients of the family are associated with the expansions of CAG repeats for Machado–Joseph disease (MJD) on the long arm of chromosome 14. Although the clinical features of MJD are very variable, general emaciation in an early stage of the disease and systemic myoclonus have not been documented. Because it is sometimes difficult to distinguish among hereditary spinocerebellar ataxias such as spinocerebellar ataxia type 1 (SCA1) or dentatorubropallidoluysian atrophy (DRPLA) by clinical features, a genetic examination provides better understanding of such a rare and ambiguous type of hereditary spinocerebellar ataxia.
Transcranial Doppler monitoring of cerebral embolism in atrial fibrillation and prosthetic valves. Clinical correlations
Authors: Anzola G. P. , Costa A. , Magoni M. , Guindani M. , Cobelli M.
Published: January 2011

Transcranial Doppler (TCD) monitoring of the middle cerebral artery (MCA) permits the detection of high intensity transient signals (HITS), which are believed to represent microemboli. Non‐valvular atrial fibrillation (NVAF) and prosthetic heart valves (PV) are important risk factors for embolic stroke. We evaluated both the prevalence and the frequency of microemboli in these high risk groups and the correlation with previous stroke. Sixty‐six patients were monitored for 30 min on both MCAs sequentially. Twenty healthy subjects were studied as well. The total number of HITS recorded on both sides, expressed as HITS/h, was used for comparison. In NVAF patients (n = 24) the prevalence of HITS was 25%, in PV (n = 16) 62% and in those patients in whom PV coexisted with atrial fibrillation (PVAF) (n = 26), it was 42%. None in the control group showed HITS. HITS occurred significantly more frequently in PVAF (12.3/h) than in both NVAF (1.4/h, p = 0.007) and PV (2.7/h, p = 0.011), whereas there was no difference between PV and NVAF. The prevalence of HITS was not statistically different in patients with and without previous stroke, but among HITS positive patients those with previous stroke had a significantly higher HITS frequency (18.9 vs 8.5/h, p = 0.04). In conclusion, in patients with cardiac embolic sources the frequency of HITS increases from the classes with the lower (NVAF, PV) to the class with the highest (PVAF) risk factor. Patients with previous stroke have more HITS than asymptomatic ones. Therefore, embolus detection monitoring seems a promising tool in the assessment of the individual stroke risk in patients with cardiac embolic sources.
Epidemiology of stroke in different regions of Siberia, Russia, 1987–1988: population‐based study in Novosibirsk, Krasnoyarsk, Tynda and Anadyr
Authors: Feigin V.L. , Wiebers D.O. , Nikitin Y.P. , Whisnant J.P. , Novokchatskaya M.V. , Belenko A.I. , Khatsenko V.N. , O'Fallon W.M.
Published: January 2011

Little information is available about stroke epidemiology in Eastern Europe. The purpose of our study was to determine and compare first‐ever stroke incidence, 30‐day case‐fatality rates, and frequency of some risk factors among stroke patients in four Siberian cities, representing western Siberia, mid‐eastern Siberia, and far eastern Siberia, Russia, during 1987–1988. There were 310 patients with first stroke in Novosibirsk, 447 in Krasnoyarsk, 51 in Tynda, and 24 in Anadyr. Age‐ and sex‐adjusted incidence of stroke was 216.1 per 100,000 residents annually in Novosibirsk, 365.4 in Krasnoyarsk, 324.2 in Tynda, and 347.7 in Anadyr; age‐ and sex‐adjusted 30‐day mortality rates were 31.9, 37.1, 22.3 and 18.3%, respectively. Among the identified patients with stroke, the prevalence of arterial hypertension was highest in Novosibirsk (79%), the prevalence of myocardial infarction and diabetes mellitus was highest in Krasnoyarsk (12 and 11%, respectively), and the prevalence of current smoking was highest in Anadyr (29%) and Tynda (28%). Age‐ and sex‐adjusted stroke incidence rates in Siberia are among the highest in the world. Stroke‐incidence rates tended to increase somewhat from west to east and from south to north across Siberia, although 30‐day mortality rates did not vary much in different regions of Siberia.
Auditory event‐related potentials before and after treatment with nasal continuous positive airway pressure in sleep apnea syndrome
Authors: Neau J.‐P. , Paquereau J. , Meurice J.‐C. , Chavagnat J.‐J. , Pinon‐Vignaud M.‐L. , Vandel B. , Recard D. , Ingrand P. , Gil R.
Published: January 2011

Auditory event‐related potentials (ERP), multiple sleep latency tests, mini‐mental state exam, and depression tests were studied in 15 patients with obstructive sleep apnea syndrome (OSA). The P3 wave latency of ERP was significantly increased compared with 15 age‐matched control subjects. After 4 weeks and after 1 year of treatment of OSA by nasal continuous positive airway pressure (CPAP), there was no significant improvement in the abnormalities of ERP. These observed changes in ERP were not correlated with excessive daytime sleepiness, depression, nocturnal hypoxemia, and sleep fragmentation. The cause of increased P3 latency has not been elucidated, but a chronic cerebral insult was suspected.
Forced vital capacity deterioration in amyotrophic lateral sclerosis has an inflexion point
Authors: Martí‐Fàbregas J. , Sanchis J. , Casan P. , Miralda R. , García‐Pachón E. , Illa I.
Published: January 2011

Serial evaluation of forced vital capacity (FVC) were performed in 34 patients with amyotrophic lateral sclerosis, 28 of whom were followed until death. Successive evaluation of FVC in the same patient did not show a linear progression. An inflexion point was detected in most patients followed to death (81%) with initial normal FVC values. The decline was more rapid and survival time was less than 1 year in most patients after the inflexion point. Significant changes in FVC were characteristic of the second half of the course of the disease. FVC results are useful for determining the presence and degree of respiratory system involvement, but our results suggest that FVC alone cannot serve as a quantitative test in clinical trials, since most patients show a curvilinear slope in FVC deterioration instead of a linear slope.
Toxoplasma gondii myelitis in AIDS
Authors: Samkoff L.M. , Daras M. , Koppel B.S. , Hirschfeld A. , Donnenfeld H.
Published: January 2011

Toxoplasmosis of the spinal cord is an uncommon manifestation of the acquired immunodeficiency syndrome (AIDS). Previously described patients generally have had poor outcomes. We report a case of successfully treated, biopsy‐proven AIDS‐related Toxoplasma gondii myelitis (TGM) in a 39‐year old man who presented with a conus medullaris syndrome. A review of the literature and a suggested therapeutic approach to TGM are presented.
Hereditary protein C deficiency associated with riboflavin‐responsive lipid storage myopathy
Authors: Vergani L. , Angelini C. , Pegoraro E. , Cadaldini M. , Simioni P. , Girolami A. , Turnbull D.M.
Published: January 2011

We report a 14 year old patient who presented lung emboli and deep vein thrombosis in relationship to protein C deficiency. He had a carnitine‐deficient lipid myopathy. Fresh muscle homogenate showed low activities in oxidizing [1‐14C]‐butyrate, [1‐14C]‐octonoate and [1‐14C]‐palmitate. A deficient short chain butyryl‐CoA dehydrogenase (SCAD) was found in isolated muscle mitochondria. The patient improved dramatically with daily therapy of 200 mg riboflavin, 2 g carnitine and anticoagulation with Coumadin. The treatment was found to restore fatty acid oxidation in fresh muscle homogenate, deficient acylCoA‐dehydrogenases in mitochondria and decrease lipid droplets.

These results suggest that in this type of lipid myopathy riboflavin supplementation may be effective. The link with protein C deficiency is discussed.
Suppression of primary writing tremor by lisuride. A case report
Authors: Torun S. , Erdinç O.
Published: January 2011

We report a patient who exhibited severe tremor in the right hand and fingers primarily while writing. Tremor showed no improvement with various medications, including proplanolol and clonazepam. Writing and drawing difficulties of the patient gradually decreased from the third week of lisuride treatment, and his tremor was totally abolished at the end of the eighth week. When he interrupted lisuride treatment for a few days, his tremor increased again over the next few days. He made the second full recovery after new treatment with lisuride. Regarding its response to a dopaminergic agonist, it may be suggested that primary writing tremor might arise in basal ganglia or related structures in the brain.
Puerperal transient cortical blindness as the only neurological manifestation of pregnancy‐induced hypertension
Authors: Leite I. , Matos I. , Braga J. , Resende J. , Monteiro L.
Published: January 2011

Transient cortical blindness in the postpartum period is a rare neurological event. Usually bilateral occipital involvement appears as a manifestation of pre‐eclampsia or eclampsia (Royburt et al., 1991; Cunningham and Lindheimer, 1992). We report a case of isolated cortical blindness as the only manifestation of pregnancy‐induced hypertension in the postpartum period.
Neuroradiological correlates of neuropsychological disorders in olivopontocerebellar atrophy (OPCA)
Authors: Botez‐Marquard T. , Pedraza O.L. , Botez M.I.
Published: January 2011

Thirty‐two OPCA patients without cortical atrophy were studied. In addition to inspection of films by a neuroradiologist (i.e. “subjective” assessment), five neuroradiological measures were used, namely, the estimation of brainstem ratio, midbrain ratio, fourth ventricular ratio, brachium pontis ratio and bicaudate ratio. The patients were divided into two groups: one with mild and the other with moderate‐severe atrophies. The neuropsychological assessment measures were: global memory quotient, verbal learning capacities, recall and recognition, attention, abstract thinking, visuo‐spatial and visuo‐constructive functioning. Three conclusions emerged: (i) cognitive disturbances in OPCA are related to the degree of cerebellar damage; (ii) these findings are consistent with the concept of anatomic and metabolic neocerebellar → basal ganglia → associative cerebral cortex loops; and (iii) it appears that the role of the neocerebellum in cognition is not exclusive because some other structures (fastigius, vermis) and the fastigial → limbic loops seem to be involved.
Pyridostigmine treatment of post‐polio syndrome fatigue: a single fibre EMG study
Authors: Girlanda P. , Nicolosi C. , Venuto C. , Mangiapane R. , Messina C.
Published: January 2011

Electrophysiological data suggest that impairment of neuromuscular junctions transmission (NMT) may be in part responsible for the fatigability affecting the majority of patients suffering with post‐poliomyelitic syndrome (PPS). The effect of the anticholinesterase medication pyridostigmine in PPS patients was evaluated by means of voluntary activation single fibre electromyography (VA‐SFEMG), a technique that is very sensitive in revealing neuromuscular transmission disturbances. Fourteen patients fulfilling the clinical criteria for PPS were included in the study. Muscle strength assessment and VA‐SFEMG were performed in basal conditions and 1 week after oral administration of pyridostigmine bromide (MESTINON) 60 mg tablet every 8 h. The treatment induced a statistically significant improvement of neuromuscular junction transmission in most PPS patients, including patients with only musculoskeletal symptoms and with post‐poliomyelitis progressive muscular atrophy. Pyridostigmine medication also produced an improvement of reported fatigue in about 70% of fatigued patients.
Primary meningeal melanocytoma of the spinal cord: report of a paediatric case with benign course and review of the literature
Authors: Kordás M. , Czirják S. , Slowik F.
Published: January 2011

A melanin producing encapsulated, intradural‐extramedullar tumour in the thoracic spinal cord was surgically removed from a 12 year old girl. The rumour histologically proved to be a melanocytoma and the patient was treated with radiation therapy. During 18 years of follow up she has been free of symptoms. The clinical and pathological features of the case and the literature are reviewed. The importance of differentiating this benign lesion from meningeal malignant pigmented tumours is emphasized.
Relationship between CSF neurotransmitter metabolites and aggressive behavior in Alzheimer's disease
Authors: Lopez O.L. , Kaufer D. , Reiter C.T. , Carra J. , DeKosky ST. , Palmer A.M.
Published: January 2011

To assess neurochemical correlates of aggressive behavior in Alzheimer's disease (AD) we examined concentrations of homovanillic acid (HVA) and 5‐hydroxyindolacetic acid (5‐HIAA) in lumbar cerebrospinal fluid (CSF) of 11 clinically diagnosed Alzheimer's disease (AD) patients and 12 non‐demented age‐equivalent controls. There were no significant differences between AD patients and controls in CSF HVA concentrations. However, the CSF 5‐HIAA content was significantly lower in AD patients compared to controls. Patients without aggressive behavior had significantly lower concentrations of HVA and 5‐HIAA than those with aggression, in whom concentrations were preserved compared to non‐demented controls.
High‐dose intravenous immunoglobulin therapy improved muscle strength in a patient with multifocal motor neuropathy and antibodies against the glycolipid LK1
Authors: Vrethem M. , Lindvall B. , Kihlstrand S. , Bäckman E. , Brismar T. , Fredman P. , Henriksson K.G.
Published: January 2011

We report improvement in muscle strength in a patient with multifocal motor neuropathy (MMN) when given high‐dose intravenous immunoglobin (i.v.‐Ig) treatment. The patient had asymmetrical limb weakness, atrophy and absent or weak reflexes, but no sensory disturbances. Neurography showed multiple conduction blocks in peripheral motor nerves but no sensory nerve abnormalities. Serum and anti‐GM1 antibodies were not found, however, the patient had serum antibodies against the glycolipid LK1, an epitope found both in glycolipid and also in some glycoproteins in peripheral nerve myelin. Muscle strength improved 5 days after i.v.‐Ig therapy, and lasted about 10 weeks. Repeated courses of treatment resulted in similar improvement. This is, to our knowledge, the first patient reported with MMN found to have antibodies against the glycolipid LK1.
Lyme Borreliosis causing severe encephalopathy and nocturnal abdominal pain in a patient with a ventriculo‐peritoneal shunt
Authors: Manto M. , Nubourgh Y. , Guillaume B. , Jacquy J.
Published: January 2011

We report the case of a 76‐year‐old patient with a previous history of normal‐pressure hydrocephalus treated with a ventriculo‐peritoneal shunting device. He was admitted one year after for severe encephalopathy and nocturnal abdominal pain. Computerized tomography (CT) of the brain showed normal ventricular size. A mild increase of protein level was present in cerebrospinal fluid (CSF). Rising levels of IgG antibodies against Borrelia burgdorferi (Bb) were detected in blood but not in CSF. Anti‐Bb IgM antibodies were not detected neither in blood nor in CSF. Abdominal investigations were all normal. Intravenous treatment with ceftriaxone was followed by a dramatic improvement We suggest making serial determinations of antibodies against Bb in patients presenting encephalopathy associated with nocturnal abdominal pain to exclude a Lyme disease. This could also avoid needless investigations and inappropriate revision of an eventual ventriculo‐peritoneal shunting device.
Post‐stroke sleep disorder treated with the selective serotonin reuptake inhibitor citalopram—a case study
Authors: Vestergaard K. , Drewes A. Mohr , Andersen G. , Taagholt S. Jørgensen
Published: January 2011

Even though stroke patients not uncommonly suffer from sleep disturbance, post‐stroke sleep disorder is one of the least studied sequela of stroke. We present a case study providing polysomnographic evidence for the successful alleviation of persistent insomnia in a non‐depressed stroke patient by treatment with the selective serotonin reuptake inhibitor citalopram. During open treatment with citalopram the patient's sleep efficiency index improved considerably, and REM latency gradually increased. Possible causes of post‐stroke insomnia are discussed, and the suggestion is made that post‐stroke sleep disorder might possibly be attributable to stroke‐induced disruption of pathways involved in the neurophysiology of sleep, e.g. serotonergic neurotransmission.
Association of levels of lipoprotein (a) and other lipoproteins with cerebrovascular disease in the Turkish population
Authors: İlhan A. , Alioǧlu Z. , Adanir M. , Özmenoǧlu Mehmet , Örem Asim
Published: January 2011

Lipoprotein (a) [Lp (a)] is a cholesterol‐rich lipoprotein that structurally resembles the low density lipoprotein cholesterol (LDL‐C) particles, but contains a molecule of apolipoprotein (a) attached to apolipoprotein B by disulfide bond. Because of the fact that high plasma levels of Lp (a) have been shown to be associated with cerebrovascular disease (CVD), we determined plasma Lp (a) levels in CVD for the Turkish population, and compared them with previous findings of some developed countries. Plasma Lp (a) levels were evaluated in CVD and control groups. The mean plasma Lp (a) levels in the CVD group was found to be approximately two‐fold higher than that of the control group (0.21 g/1 vs 0.38 g/1). Also, it was found to be higher than the mean levels of CVD group in the other populations described in previous reports. But CVD prevalence in the Turkish population is lower than in those of developed countries, especially United States and Japan. Therefore, we believe that each of those populations should determine their plasma Lp (a) levels to observe the risk for CVD.
Memory function during low intensity hippocampal electrical stimulation in patients with temporal lobe epilepsy
Authors: Fernández G. , Hufnagel A. , Helmstaedter C. , Zentner J. , Elger C.E.
Published: January 2011

Hippocampal memory dysfunction is a main symptom of mesiotemporal lobe epilepsy (TLE). It may increase after temporal lobectomy for seizure relief. The aim of this study was to assess the ability of psychometry during hippocampal electrical stimulation to predict post‐operative memory deficits and thereby to contribute to lateralization of the epileptogenic zone. A computerized memory test was performed during low intensity hippocampal stimulation in nine patients with TLE during invasive presurgical evaluation. The following results were obtained: speech dominant hippocampal stimulation induced subtle verbal memory deficits in patients with the epileptogenic zone in the speech dominant hemisphere and normal baseline memory performance. Verbal memory deficits could not be induced in patients with the epileptogenic zone in the speech dominant hemisphere and pre‐existing memory deficits, or if the seizure origin was contralateral to speech dominance. Thus it was possible to lateralize the epileptogenic zone in patients with normal baseline memory performance by revealing hippocampal dysfunction only during electrical stimulation. Post‐operative psychometric testing demonstrated that the individual risk for impairment of verbal memory performance following temporal lobectomy could be predicted correctly. In conclusion, psychometry during hippocampal stimulation may allow prediction of memory deficits following temporal lobectomy and improve determination of the epileptogenic zone.
Quantitative EEG changes in non‐demented Parkinson's disease patients before and during L‐dopa therapy
Authors: Stanzione P. , Marciani M.G. , Maschio M. , Bassetti M.A. , Spanedda F. , Pierantozzi M. , Semprini R. , Bernardi G.
Published: January 2011

Nineteen non‐demented Parkinson's disease patients have been studied before and during L‐dopa therapy by quantitative EEG performed at rest with eyes closed (EC) and during attentive (BR) and cognitive (FIX) tasks. The data have been compared by ANOVA analysis with those of 22 age‐matched healthy subjects. In all three conditions a significant increase of the mean δ power as well as a decrease of β1 power was observed in patients before therapy. Abnormal high δ values were observed in 10 out of 19 patients. L‐Dopa therapy did not modify this EEG pattern. After therapy, however, a significant decrease of reactivity to BR and FIX was observed in patients compared to normal subjects. These data confirmed the presence of an EEG synchronization (increase of slow activity and decrease of fast activity) in non‐demented Parkinson's disease patients. This pattern, similar to that of subjects with Alzheimer‐type dementia, might indicate an intellectual impairment at sub‐clinical level. A non‐dopaminergic mechanism could be responsible for this impairment
Platelet phenolsulphotransferase activity in patients with dementia of Alzheimer type
Authors: Bongioanni P. , Donato M. , Castagna M. , Gemignani F.
Published: January 2011

Human blood platelets are more and more regarded as a reliable model of nerve cells, and some biochemical alterations found in platelet enzyme activities and receptor binding parameters may be related to analogous changes occuring in the central nervous system. Platelet phenol‐sulphotransferase activity has been evaluated in some neurological disorders, such as Parkinson's disease and headache. In the present work we determined phenolsulphotransferase activity in platelets of 36 patients with dementia of Alzheimer type, and compared such activity values with those of 36 sex‐ and age‐matched healthy controls. Patients showed a significantly higher platelet phenolsulphotransferase activity than control subjects, both with dopamine and with phenol as substrates. Moreover, a significant positive correlation was found between platelet enzyme activity and severity of illness. These findings are discussed in terms of the biochemical abnormalities found in the central nervous system of demented subjects, and in terms of the possible pathogenetic involvement of an altered phenolsulphotransferase activity (and, in general, of a modified monoamine metabolism) in such derangements of biochemical systems often occuring in dementia of Alzheimer type.