Dementia is relatively frequent after a clinical first stroke in persons younger than 80 years, and aphasia is very often associated with poststroke dementia. If aphasic patients are not considered, it may be necessary to screen a very large number of subjects to collect an adequate sample of demented cases.

Objectives: Hepatitis C virus (HCV) infection is often associated with cryoglobulinaemia (CG). Peripheral neuropathy (PN) is a comparatively common complication of CG associated with HCV infection and it is thought to be attributable to nerve ischaemia. Only few HCV CG patients with PN have been reported. The recent finding of HCV RNA in nerve biopsy specimens has suggested a possible direct role of HCV in the pathogenesis of PN. The authors studied 51 HCV patients to determine the prevalence of CG and to clarify the possible mechanism by which HCV determines the PN. Methods: All the patients were studied clinically, by laboratory tests and electrophysiologically. Twenty eight patients underwent sural nerve biopsy where both morphological and morphometric evaluation of the biopsy specimen was performed, as well as statistical analysis. Results: CG was found in 40 of 51 cases (78%). Polyneuropathy was significantly prevalent in CG+ patients compared with CG− (18 of 40 compared with 1 of 11 patients; p=0.01). HCV CG− patients more frequently developed well defined mononeuropathy or multiple neuropathy when compared with HCV CG+ (10 of 11 compared with 22 of 40; p<0.03). HCV CG+ patients showed significantly higher proportion of rheumatoid factor positivity (p<0.001) and low C4 levels (p=0.001). Nerve biopsy was performed in 25 of 40 HCV CG+ patients and in 3 of 11 HCV CG− patients: epineurial vasculitis was present in 8 of 25 HCV CG+ (32%) and in 2 of 3 HCV CG−. Differential fascicular loss of axons was found in 10 of 25 CG+ (40%) and 1 of 3 CG−, signs of both demyelination and axonal degeneration were present in 7 of 25 CG+ (28%). No significant difference was found in neuropathological features, while histometrical analysis disclosed more severe involvement in CG+ patients. Conclusions: These findings suggest that the presence of CG is a negative predictive factor for the associated PN. Morphological findings in the sural nerve from HCV CG− and CG+ are consistent with an ischaemic mechanism of nerve damage and are against a direct role of the virus in causing the associated PN.

Background and Purpose: We aimed to investigate the rate of hospital admissions for cerebrovascular events and of revascularization treatments for acute ischemic stroke in Italy during the coronavirus disease 2019 (COVID-19) outbreak. Methods: The Italian Stroke Organization performed a multicenter study involving 93 Italian Stroke Units. We collected information on hospital admissions for cerebrovascular events from March 1 to March 31, 2020 (study period), and from March 1 to March 31, 2019 (control period). Results: Ischemic strokes decreased from 2399 in 2019 to 1810 in 2020, with a corresponding hospitalization rate ratio (RR) of 0.75 ([95% CI, 0.71–0.80] P <0.001); intracerebral hemorrhages decreased from 400 to 322 (hospitalization RR, 0.81 [95% CI, 0.69–0.93]; P =0.004), and transient ischemic attacks decreased from 322 to 196 (hospitalization RR, 0.61 [95% CI, 0.51–0.73]; P <0.001). Hospitalizations decreased in Northern, Central, and Southern Italy. Intravenous thrombolyses decreased from 531 (22.1%) in 2019 to 345 in 2020 (19.1%; RR, 0.86 [95% CI, 0.75–0.99]; P =0.032), while primary endovascular procedures increased in Northern Italy (RR, 1.61 [95% CI, 1.13–2.32]; P =0.008). We found no correlation ( P =0.517) between the hospitalization RRs for all strokes or transient ischemic attack and COVID-19 incidence in the different areas. Conclusions: Hospitalizations for stroke or transient ischemic attacks across Italy were reduced during the worst period of the COVID-19 outbreak. Intravenous thrombolytic treatments also decreased, while endovascular treatments remained unchanged and even increased in the area of maximum expression of the outbreak. Limited hospitalization of the less severe patients and delays in hospital admission, due to overcharge of the emergency system by COVID-19 patients, may explain these data.

SUMMARY Clinical, neurophysiological and morphological studies of four patients with polyneuropathy and secondary hypothyroidism are reported. Neurophysiological studies revealed signs of muscle denervation and reduction of conduction velocity in all the patients. Sural nerve biopsies showed axonal degeneration in all cases but one. All the patients were treated with replacement therapy and clinical symptomatology and neurophysiological parameters improved in all patients.In the literature two types of abnormality of the peripheral nervous system in hypothyroidism have been described. The first is a mononeuropathy, due to mucinous deposits which cause nerve damage through a compression mechanism;' the second is a sensorimotor polyneuropathy. Morphologically, some studies have shown a primary involvement of myelin,2 3 while more recent studies have shown primary axonal damage.4 5 The present report deals with four patients with sensorimotor polyneuropathy associated with hypothyroidism. These patients were treated by substitution therapy and followed clinically and electrophysiologically until achievement of the euthyroid state. mal. Laboratory data were normal except for a moderate normochromic and normocytic anaemia. CK and LDH were normal. T3 was 0-2 ng/ml (normal 06-2 0 ng/ml), T4 was 13 ng/ml (normal 65-130 ng/ml); TSH was 63-3 IU/ml (normal 2-7IU/ml). Antimicrosomal, antismooth muscle and antigastric wall antibodies were found. Ultrasound and scintiscanning showed a small thyroid gland with poor uptake. The diagnosis was Hashimoto's thyroiditis.Patient 2 E.B., a 58 year old woman, was admitted because of a 5 month history of weakness and paraesthesia in upper and lower limbs. There was no significant past history, except for recent constipation. The general examination showed a dry and cold skin, alopecia on the outer third of the eybrows and a goitre. Neurological examination disclosed dysarthria, slight weakness of all four limbs, especially in the distal muscles of the legs. Knee and ankle reflexes were depressed. She had widebased standing and her gait was slightly ataxic. There was no sensory impairment. Laboratory data were normal except for T3 0-8 ng/ml; T4 12ng/ml and TSH 35-1 IU/ml. Organ specific autoantibodies were absent. Thyroid scintiscanning showed a reduced uptake of radioisotope Tc 99. Patient 3 E.M., a 58 year old man, was seen 2 years after the onset of weakness in the proximal muscles of the legs, distal cramps caused by exposure to cold and fasciculation. A subacute thyroiditis had been diagnosed 4 years before. Neurological examination revealed mild deterioration of higher cerebral functions, dysarthna and scanning speech. The only abnormalities in the upper limbs were reduced tendon reflexes. In the legs, both bulk and strength were reduced, with slight atrophy of both quadriceps muscles and fasciculation. Knee and ankle jerks were absent. Touch and vibration sensations were slightly diminished in all four limbs. Laboratory investigations showed normochromic

Background and Purpose-Heparin is widely used for acute stroke to prevent thrombus propagation and/or multiple emboli generation, although there is, as yet, no demonstrated efficacy. However, all of the available clinical studies allowed long intervals from stroke to treatment. The purpose of this study was to try an intravenous regimen of unfractionated heparin the acute cerebral infarction starting treatment within the first 3 hours of the onset of symptoms. Methods-The study was an outcome evaluator-blind design trial. Patients had to display signs of a nonlacunar hemispheric infarction. Selected patients were randomly allocated to receive intravenous heparin sodium or saline.Heparin was infused at a rate to maintain activated partial thromboplastin time ratio 2.0 to 2.5 ϫ control for 5 days. The primary end point was recovery of a modified Rankin score zero to 2 at 90 days of stroke at phone interview by a single physician blind to treatment. Safety end points were death, symptomatic intracranial hemorrhages, and major extracranial bleedings by 90 days of stroke. Results-A total of 418 stroke patients were included. In the heparin group, there were more self-independent patients (38.9% versus 28.6%; Pϭ0.025). In addition, in the same group, there were fewer deaths (16.8% versus 21.9%; Pϭ0.189), more symptomatic brain hemorrhages (6.2% versus 1.4%; Pϭ0.008), and more major extracerebral bleedings (2.9% versus 1.4%; Pϭ0.491). Conclusions-Intravenous heparin sodium could be of help in the earliest treatment of acute nonlacunar hemispheric cerebral infarction, even keeping into account an increased frequency of intracranial symptomatic brain hemorrhages.

In an Italian population of 275 unrelated men affected by adult-onset sporadic progressive cerebellar ataxia, the authors found six patients carrying an FMR1 gene premutation. Age at onset (range, 53 to 69 years) and clinical-neuropathologic findings were consistent with the fragile-X tremor ataxia syndrome (FXTAS), although tremor was not as common as previously described. FXTAS accounted for 4.2% of the cases diagnosed at >50 years, suggesting that it is a frequent genetic cause of late-onset sporadic ataxia.

Background and Purpose:We sought to detect prognostic factors related to functional outcome during the first 6 hours after a first-ever stroke in the carotid artery territory.Methods: All patients with these characteristics seen during a 3-year period were included. Outcome was evaluated according to a modified Rankin scale. The following variables were examined at univariate analysis: sex, age, severity of deficit at entry and at day 7, level of consciousness at entry, time after symptom onset, history of smoking, history of hypertension, diabetes, myocardial infarction, atrial fibrillation, rheumatic heart disease, dilated cardiomyopathy, all potential cardioembolic sources, presence of a consistent lesion on computed tomography at entry and at days 5-9, and the size of such lesion.Results: All entry criteria were met by 172 patients. Age >70 years, a Canadian Neurological Scale score <6.5 at entry and at day 7, atrial fibrillation, presence of a potential cardioembolic source, and a "large" lesion (involving more than half the cerebral lobe) on computed tomography at days 5-9 were associated with a significantly worse outcome both at 30 days and at 6 months. After multivariate analysis, a Canadian Scale score <6.5 at entry (/J<0.0001) and atrial fibrillation (p=0.005) were associated with a significant handicap or death at 30 days, whereas only a Canadian Scale score <6.5 (p<0.0001) was associated with a worse prognosis at 6 months. An association of age >70 years with a worse outcome at 6 months was of borderline significance (jp=0.054).Conclusions: Some prognostic indicators are available during the first few hours after onset of a carotid ischemic stroke and may be useful in the stratification of patients in clinical trials. Severity of deficit is the most important indicator, whereas the presence of atrial fibrillation worsens the prognostic outlook with respect to early handicap but not mortality.

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