Search

Background: Epilepsy and hypertension are common chronic conditions, both showing high prevalence in older age groups. This review outlines current experimental and clinical evidence on both direct and indirect role of hypertension in epileptogenesis and discusses the principles of drug treatment in patients with hypertension and epilepsy. Methods: We selected English-written articles on epilepsy, hypertension, stroke, and cerebrovascular disease until December, 2018. Results: Renin-angiotensin system might play a central role in the direct interaction between hypertension and epilepsy, but other mechanisms may be contemplated. Large-artery stroke, small vessel disease and posterior reversible leukoencephalopathy syndrome are hypertension-related brain lesions able to determine epilepsy by indirect mechanisms. The role of hypertension as an independent risk factor for post-stroke epilepsy has not been demonstrated. The role of hypertension-related small vessel disease in adult-onset epilepsy has been demonstrated. Posterior reversible encephalopathy syndrome is an acute condition, often caused by a hypertensive crisis, associated with the occurrence of acute symptomatic seizures. Chronic antiepileptic treatment should consider the risk of drug-drug interactions with antihypertensives. Conclusions: Current evidence from preclinical and clinical studies supports the vision that hypertension may be a cause of seizures and epilepsy through direct or indirect mechanisms. In both post-stroke epilepsy and small vessel disease-associated epilepsy, chronic antiepileptic treatment is recommended. In posterior reversible encephalopathy syndrome blood pressure must be rapidly lowered and prompt antiepileptic treatment should be initiated.

Background REM-sleep behavior disorder (RBD) therapy is based on small to medium-sized case series, as no large controlled clinical trials have been performed. The most used and widely recognized effective drugs are clonazepam and melatonin, with anecdotal reports on the potential benefit of other drug classes. Methods We report on two patients suffering from idiopathic RBD presenting with almost nightly complex and violent episodes, refractory to conventional drugs. Both patients, after informed consent, were treated off-label with sodium oxybate in add-on therapy. We followed up the patients in order to assess treatment efficacy by means of clinical interview, visual analog scales (VAS) for frequency and severity, Clinical Global Impression (CGI) improvement scale and efficacy index, video-polysomnography and at-home actigraphy. Results Sodium oxybate intake was well tolerated and effective in reducing the number and intensity of RBD episodes; patients reported no new traumatic episodes. Results were confirmed by bed-partner reports, VAS, CGI improvement scale and efficacy index, and at-home actigraphic monitoring, the latter showing a trend of improvement in nocturnal sleep quality and reduction in motor activity, compared to the baseline. Nevertheless, video-polysomnography did not show a clear beneficial effect on sleep-related electromyographic parameters. Conclusions Our cases suggest that sodium oxybate can be an effective add-on option for the treatment of idiopathic RBD refractory to conventional therapies. The lack of improvement of polysomnographic parameters suggests caution in considering only polysomnographic data as endpoints in the assessment of the efficacy of therapies for RBD, and that long-term home-based assessment seems a promising tool.

The document deals with some ethical issues raised by the treatment of demented people. In particular the conceptual and empirical aspects of the assessment of awareness and competence of these patients are analysed, as well as the dilemmas related to the treatment of behavioral disorders.

Mycophenolate mofetil (MM) is a new generation immunosuppressant, which has been successfully used for treatment of renal, heart and liver transplants, and other immune-mediated diseases. MM is also a safe and steroid-sparing agent for treating neuromuscular diseases, like chronic inflammatory demyelinating neuropathy and myastenia gravis. MM is an ester of mycophenolic acid, an agent that inhibits the proliferation of B and T lymphocytes. Side effects are modest and there is a lower risk for late malignancies than other immunosuppressive drugs. We assessed MM in the treatment of multifocal motor neuropathy (MMN). The therapy of MMN largely depends upon the use of intravenous immunoglobulins (IVIg). IVIg induce and maintain improvement in MMN, but they do not eradicate the disease and are very expensive. No randomized controlled trials are available to indicate whether immunosuppressive agents are beneficial in MMN. We treated with MM four patients who fulfilled the clinical, laboratory and electrodiagnostic criteria for MMN, aiming to assess whether the drug is safe and may help in reducing or discontinuing IVIg infusion in this disease. MM administration, at 1 g twice daily, was started when patients were still under IVIg treatment and showed minimal or no disability, as judged by the INCAT disability scale. At the third month of MM therapy, IVIg infusion was discontinued in 2 patients and reduced by 20 % in 2 patients. After a follow up ranging from 1 to 6 months, no worsening in the INCAT disability scale was observed in all the patients. One patient discontinued the medication after four months because of gastrointestinal discomfort with diarrhea, weight loss and increased amylase/lipase levels. The promising response to MM and the lack of major side effects, warrant further multicentric controlled trials in MMN.

STUDY OBJECTIVES: REM sleep behavior disorder (RBD) can be induced by antidepressants, especially serotonin reuptake inhibitors (SSRI), thus a role of the serotonergic system in the pathogenesis of RBD has been proposed. However, the serotonergic system integrity in idiopathic RBD (iRBD) is still unknown. We aimed to study brain stem serotonergic system integrity, by means of (123)I-FP-CIT-SPECT, in a group of iRBD patients as compared to normal subjects. DESIGN: Single-center, prospective observational study. SETTING: University hospital. PATIENTS OR PARTICIPANTS: Twenty iRBD outpatients and 23 age-matched normal controls. MEASUREMENTS AND RESULTS: The diagnosis of RBD was determined clinically and confirmed by means of overnight, laboratory-based video-polysomnography. Both iRBD patients and normal subjects underwent (123)I-FP-CIT-SPECT as a marker of dopamine transporter (DAT) at basal ganglia level and of serotonin transporter (SERT) at brainstem and thalamus levels. (123)I-FP-CIT-SPECT images were analyzed and compared between iRBD patients and controls by means of both region of interest analysis at basal ganglia, midbrain, pons and thalamus levels, and voxel-based analysis, taking into account age and the use of SSRI as confounding factors. No difference in (123)I-FP-CIT-SPECT specific to nondisplaceable binding ratios (SBR) values was found between iRBD and normal subjects at brainstem and thalamus levels while iRBD patients showed lower SBR values in all basal ganglia nuclei (P < 0.0001) compared to controls. CONCLUSIONS: These results suggest that the serotonergic system is not directly involved in RBD pathogenesis while confirming nigro-striatal dopaminergic deafferentation in iRBD.

Background:Ifosfamide (IFX), an alkylating agent and isomer of cyclophosphamide, is used as a single agent or a component of multi-agent chemotherapy in the treatment of ovarian, testicular, head and neck cancers, sarcomas and lymphomas. Encephalopathy is manifested by cerebellar ataxia, confusional state, complex visual hallucinations, extrapyramidal signs, seizures, and mutism.Case reports:We report two patients with non-Hodgkin’s lymphoma presenting with mutism and confusional state after IFX infusion. Nonconvulsive status epilepticus (NCSE) as the cause of confusion was diagnosed on the basis of EEG pattern and the apparent improvement following intravenous administration of diazepam.Conclusions:Electroencephalogram abnormalities during IFX treatment have been described but recordings are only available in six cases. In three of them, paroxysmal alterations warranted the diagnosis of NCSE; however, most cases of IFX encephalopathy might have associated NCSE.

In 13 patients who experienced transient global amnesia (TGA), quantified electroencephalographic (qEEG) records were carried out within 1 week of the episodes, and compared with those in 13 cases with cerebral transient ischemic attacks (TIA), and 13 normal controls, matched for age and sex. A statistical comparison of the absolute power showed few differences between TGA and TIA patients, and many statistical differences between TGA patients and controls. The qEEG pattern reveales an involvement of the temporo-parietal structures in TGA patients. These findings suggest the presence of subclinical sequelae, after the TGA attack.

In anoxic coma, myoclonic status epilepticus and other nonreactive epileptiform patterns are considered as signs of poor prognosis. We report the case of a good recovery in a prolonged comatose myoclonic status epilepticus (MSE) after a cardiac arrest (CA) treated with mild therapeutic hypothermia (TH) in a patient who had undergone a bone marrow transplantation for Hodgkin's lymphoma. This case emphasizes the opportunity of performing an electroencephalogram (EEG) in the acute period after an hypoxic-ischemic insult and underlines the diagnostic difficulties between MSE and Lance-Adams syndrome, which classically occurs after the patient has regained consciousness, but can also begin while the patient is still comatose or sedated. Major problems in prognostication for postarrest comatose patients will also be pointed out.

Chronic Fatigue Syndrome (CFS) represents a disabling condition characterized by persistent mental and physical fatigue, bodily discomfort and cognitive difficulties. To date the neural bases of CFS are poorly understood; however, mono-aminergic abnormalities, sleep-wake cycle changes and prefrontal dysfunctions are all thought to play a role in the development and maintenance of this condition. Here we explored in a group of 62 CFS subjects the impact on fatigue levels of agomelatine, an antidepressant with agonist activity at melatonin receptors (MT1 and MT2) and antagonist activity at serotoninergic 2C receptors (5HT2C). To tease out the relative effects of MT-agonism and 5HT2C antagonism on fatigue, we compared agomelatine 50mg u.i.d. with sustained release melatonin 10mg u.i.d. in the first 12-week-long phase of the study, and then switched all melatonin-treated subjects to agomelatine in the second 12-week-long phase of the study. Agomelatine treatment, but not melatonin, was associated with a significant reduction of perceived fatigue and an increase in perceived quality of life. Moreover the switch from melatonin to agomelatine was associated with a reduction of fatigue levels. Agomelatine was well tolerated by all enrolled subjects. Our data, albeit preliminary, suggest that agomelatine treatment could represent a novel useful approach to the clinical care of subjects with CFS.

Levofloxacin is a third generation fluorinated quinolone ntibiotic with a broad spectrum of antibacterial activity. It s generally well tolerated, with a very low rate of clinially important neurological adverse events. Fluoroquinolonessociated neurotoxicity may manifest as seizures, delirium or ncephalopathy. Here we describe the first case of levofloxacinnduced NCSE in a woman without history of neurological iseases.

Different pharmacologic agents have been evaluated in the treatment of Chronic Fatigue Syndrome (CFS), albeit with moderate efficacy. Among the compounds thought to present with potential to be efficacious in CFS patients stands out low-dose amisulpride, a substituted benzamide that has been shown to be an useful treatment for conditions which exhibit some overlap with CFS such as dysthymia and somatoform disorders. We thus recruited forty non-depressed CFS patients that were randomized to receive either amisulpride 25mg bid, or fluoxetine 20mg uid; all subjects were un-blinded to the treatment regimen. At the time of enrollment in the study and after twelve weeks of treatment, enrolled subjects completed the Krupp Fatigue Severity Scale, the Hospital Anxiety and Depression Scale and a visual analog scale focused on pain and bodily discomfort. Moreover, all subjects were evaluated by a clinician, blinded to the treatment regimen, using the Clinical Global Impression Severity Scale. Our data revealed a significant improvement both in self-report, and observer-based measures for the amisulpride-treated, but not for the fluoxetine-treated patients. Amisulpride-treated subjects also presented with a significant reduction of somatic complaints, while the amisulpride effect on anxiety and mood levels was not significant. Both drugs were equally well tolerated. Summing up, we showed a positive symptomatic effect of amisulpride, compared to SSRI treatment, in a group of non-depressed CSF patients on self-report and on observer-based measures of fatigue and somatic complaints. If confirmed by larger, blinded studies, amisulpride thus could represent an effective approach to this difficult-to-treat condition.

Recurrent episodes of transient neurological dysfunction occurring in a patient with evidence of recent multiple lacunar infarctions were at first diagnosed as transient ischemic attacks (TIAs), but later proved to be due to focal inhibitory seizures. The differential diagnosis between TIAs and partial epileptic seizures in patients with ischemic cerebrovascular disease may sometimes be difficult in the presence of uncommon clinical manifestations.

We report a case of crossed aphasia in a strongly right-handed woman due to a parieto-occipital tumor in the right hemisphere, documented by CT and MR images. Neuropsychological assessment was conducted on four different occasions: results revealed an uncommon feature in our case, because of the nature of the lesion and the evolution of the clinical picture. These findings are discussed in relation to the literature.

The relationship between depression and dementia in Parkinson's disease (PD) has rarely been explored. Using a quantitative EEG (qEEG) parameter, we studied four groups of subjects: PD, demented Alzheimer's type and major depressed patients and normal controls. The qEEG data were compared with those of the Mini-Mental State and the Hamilton Depression Scale. The qEEG pattern was different in the four groups of subjects. Moreover, there was a significant correlation between the qEEG data and the other variables, and, particularly, with the cognitive performances. Our findings demonstrate that the qEEG method of assessment may give valuable data for a better classification of dementia syndromes and for a distinction between dementia and pseudodementia.

A long-term follow-up study was performed on patients with transient global amnesia (TGA) in order to evaluate the prognosis, the recurrence rate and the occurrence of stroke and dementia. 102 patients (57 women, 45 men; mean age 62.8 +/- 9.4 years) were prospectively included and followed up. The follow-up duration ranged between 12 and 241 months with an average value of 82.2 +/- 51.1 (mean +/- SD). The death rate showed no difference from that of sex- and age-matched subjects. TGA recurred in 19 cases (18.63%). Only 4 patients suffered subsequent stroke, and only 3 showed intellectual deterioration. TGA prognosis was shown to be better than that of RIA and lacunar patients.

Neurosyphilis is still a significant medical problem in developing countries and syphilitic ocular manifestations are often not diagnosed due to the lack of typical characteristics. We describe the case of a 59-year-old homosexual man with a 1-month history of decreased vision acuity in his left eye who was diagnosed with neurosyphilis and received treatment with intravenous penicillin G (16 million units in divided daily doses), with great improvement of visual acuity and CSF examination findings. The interest of this case is not only represented by the unusually early ocular involvement, but also by the rapid evolution of the disease into the secondary stage in a man who had had one at-risk homosexual relationship only 3 months before the onset symptoms. We also support the view that the presence of ocular involvement in syphilitic patients is suggestive of involvement of the CNS and should be considered synonymous with neurosyphilis.

The quantified electroencephalogram (qEEG) of patients with senile dementia of the Alzheimer type (SDAT) and normal elderly subjects was related to the Mini-Mental State (MMS) score. A statistically significant correlation was observed between MMS score and some qEEG parameters. This correlation indicates that the use of adequate spectral parameters of qEEG may provide information on the cognitive impairment of elderly subjects and may reduce the false-positive rate at a neuropsychological examination.

Although the incidence of seizures in neurosyphilis ranges from 14 to 60%, status epilepticus (SE) as a presenting complaint of neurosyphilis is definitely rare. A 44-year-old human immunodeficiency virus (HIV)-negative man with no history of epilepsy suddenly presented with acute mental confusion and was diagnosed as having a de novo complex partial nonconvulsive SE. Cerebrospinal fluid (CSF) findings, neuroimaging, and clinical course indicated that SE was the presenting symptom of an undiagnosed syphilitic meningovasculitis. The case is presented with a review of previous reports to emphasize the differential features and to underscore the importance of considering neurosyphilis among the possible causes of de novo SE.

We describe two patients with Parkinson's disease (PD) who developed clinical criteria of pathological gambling addiction in the setting of increased dopamine replacement therapy (levodopa and dopamine agonist medications). The second patient showed also signs of dopamine dysregulation syndrome, with an addiction to dopaminergic medication. Neither patients responded to the standard therapy for gambling behavior, but dramatically improved after bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) and early postoperative withdrawal of dopaminergic therapy. The possible therapeutic role of subthalamic nucleus deep brain stimulation (STN-DBS) on such a disabling behavior needs to be investigated prospectively.

Cephalosporins may induce nonconvulsive status epilepticus (NCSE), a potentially reversible condition. Despite the wide use of these antibiotics, there are only few reported cases, because this condition is probably underestimated. We report two new cases of NCSE occurring during treatment with cefepime and ceftazidime, and emphasize the utility of emergent electroencephalogram in patients with an acute altered state of consciousness while receiving treatment with cephalosporins, particularly when there is evidence of impaired renal function.

A. Brusa1 ( ) • A.R. Bentivoglio2 • S. Calzetti3 S. Cammarata4 • S. Congia5 • A. Fasano2 B. Jandolo6 • B. Lucci7 • A. Primavera8 • R. Stoehr4 1 Ospedale Galliera, Genoa, Italy 2 Istituto di Neurologia, Universita Cattolica del Sacro Cuore, Rome, Italy 3 Istituto di Neurologia, Universita degli Studi di Parma, Parma, Italy 4 Divisione Neurologica, Ospedale Galliera, Genoa, Italy 5 Cattedra di Neurofisiopatologia, Universita di Cagliari, Italy 6 Dipartimento di Neuroscienze e Patologia Cervico-Facciale, Istituto Regina Elena, Rome, Italy 7 U.O.D. Neurologia Azienda Ospedaliera S. Maria degli Angeli, Pordenone, Italy 8 Dipartimento di Scienze Neurologiche e Neuroriabilitazione, Clinica Neurologica dell’Universita di Genova, Genoa, Italy

OBJECTIVES—Reversible posterior leucoencephalopathy syndrome (RPLS) may develop in patients with renal insufficiency, hypertension, and immunosuppression, and is managed by prompt antihypertensive and anticonvulsant treatment. Four patients with renal insufficiency and fluid overload associated with Wegener's granulomatosis (one patient) and systemic lupus erythematosus (SLE) (three patients) are described, whose clinical picture and neuroimaging indicated RPLS. CASE REPORTS—All patients had headache, seizures, visual abnormalities, and transient motor deficit, and were hypertensive at the onset of the symptoms. Head computed tomography (CT) scan and magnetic resonance imaging showed predominantly posterior signal abnormalities, which were more conspicuous on T2 weighted spin echo images than on CT scan. All patients had some form of cytotoxic treatment shortly before the syndrome developed, and dramatically responded to blood pressure control and anticonvulsant treatment. In two patients with SLE, dialysis was required for renal insufficiency. DISCUSSION—Follow up neuroimaging studies showed almost complete resolution of signal abnormalities, and suggested that RPLS was associated with cerebral oedema without concomitant infarction. The treatment of hypertension and neurotoxic condition such as uraemia appears of primary importance, while immunosuppressive treatment may cause further damage of the blood-brain barrier.

We describe two Italian first cousins with familial amyloidotic polyneuropathy associated with transthyretin variant consisting of the substitution of alanine for glycine at codon 47 (TTR Ala-47), from a family with a history of cardiac failure. The 40-year-old patient presented with autonomic dysfunction and the 44-year-old cousin with congestive heart failure. Both developed sensorimotor and autonomic polyneuropathy. Since a similar clinical picture has been described in another Italian family, the cardiac involvement must be regarded as a salient and early feature of the TTR Ala-47 mutation.

The tau gene has been found to be the locus of dementia with rigidity linked to chromosome 17. Exonic and intronic mutations have been described in a number of families. Here we describe a P301S mutation in exon 10 of the tau gene in a new family. Two members of this family were affected. One individual presented with frontotemporal dementia, whereas his son has corticobasal degeneration, demonstrating that the same primary gene defect in tau can lead to 2 distinct clinical phenotypes. Both individuals developed rapidly progressive disease in the third decade. Neuropathologically, the father presented with an extensive filamentous pathology made of hyperphosphorylated tau protein. Biochemically, recombinant tau protein with the P301S mutation showed a greatly reduced ability to promote microtubule assembly.

To the Editor: We read with interest the article by Panayiotopoulos et al.1 reporting two patients with idiopathic generalized epilepsy in whom vigabatrin increased the frequency and severity of absences and absence status. We recently observed a case of "de novo" absence status soon after the addition of vigabatrin to the current antiepileptic regimen. A 28-year-old man with perinatal cerebral damage due to prolonged asphyxia had onset at age 3 years of generalized tonic-clonic seizures and short-lasting spells of consciousness impairment with automatisms. CT and MRI of the brain were normal. Repeat interictal EEGs showed bursts of 3 to 5 Hz sharp waves and brief atypical spike and polyspike …

To the Editor: Treatment of symptomatic neurosyphilis is an increasingly common clinical problem because of its rising incidence, particularly in patients coinfected with the human immunodeficiency virus type 1 (HIV-1).1 The mainstay of treatment remains intravenous penicillin G at high dosage, ranging from 12 million to 24 million units given six times a day for 10 to 14 days.1 Treatment options for patients with neurosyphilis who are allergic to penicillin are limited. Such patients should undergo a skin test and hospitalization for a penicillin-desensitization protocol before intravenous penicillin administration.2,3 We know little, however, about the outcomes of high-dose penicillin . . .

Aphasia due to simple partial status epilepticus is rare. We report a case of prolonged mixed aphasia without clouding of consciousness in a patient with an old history (10 years) of multiple sclerosis (MS). We found a clear clinical-EEG correlation with a continuous epileptic pattern in the shape of periodic lateralized epileptiform discharges (PLEDs). Clinical, laboratory and neuroradiological data ruled out possible etiological conditions other than MS and suggested that the development of new subcortical demyelinating lesions might play a critical role in seizure production. These findings, besides the role of PLEDs as an intrinsic feature of the status epilepticus condition, are discussed in relation to the literature.

Acute catatonic syndrome is a condition that can be caused by a variety of metabolic, neurological, psychiatric, and toxic conditions, including neuroleptic malignant syndrome. Although ictal catatonia as a manifestation of non-convulsive status epilepticus has been described, reference to the occurrence of seizures in patients with acute catatonic syndrome is anecdotal. Twenty nine patients with acute catatonic syndrome were reviewed to identify patients with seizures after the onset of acute catatonic syndrome. Patients were divided into four diagnostic groups: affective (15), schizophrenic (eight), toxic (two), and organic (four). Seizures occurred in four patients (13.8%): two patients with dystonic seizures had viral encephalitis and schizophrenic disorder respectively; one patient with complex partial seizures had viral encephalitis and one patient with absence status had neuroleptic malignant syndrome. The results indicate the value of EEG in detection of epileptic activity in patients with acute catatonic syndrome, both at onset and in the course of such disturbance, particularly to provide a differential diagnosis between pseudo-seizures and neuroleptic-induced acute dystonia.

Five patients (4 women, 1 man) presented with an acute confusional episode for the first time between the ages of 53 and 76. Their EEGs showed generalized paroxysmal activity indicating a diagnosis of nonconvulsive generalized status epilepticus (absence status). Two patients had tonic-clonic seizures just before the onset of the status, but none had a history of chronic epilepsy. Three patients had long-standing psychiatric disorders. Treatment with psychotropic drugs and medical illness (vascular disease, metabolic derangement) may have acted as precipitating factors for the status epilepticus in all patients. The diagnosis was never made on admission, since psychiatric history and ictal behavioral manifestations often raised intriguing problems of differential diagnosis. In all cases, only icta; EEG could provide a correct diagnostic assessment.

Wernicke-Korsakoff disease with sensory-motor neuropathy was diagnosed in three out of a series of 1,663 patients (0.18%), with onset 2, 3 and 5 months after biliopancreatic diversion. Precipitating factors were vomiting, minimal food intake, anorexia, rapid weight loss, and glucose-containing intravenous feeding. Recovery was partial in two and complete in one of the patients. In the early postop, prophylactic thiamine should be given to the patients with excessively limited eating capacity. Larger doses of thiamine should be instituted parenterally either in the case of suspected Wernicke-Korsakoff encephalopathy or before starting feeding for protein malnutrition.

Objectives: Recent interest has been expressed in peripheral neuropathies in hepatitis C virus (HCV) patients. The aim of this prospective study was to evaluate the prevalence of peripheral neuropathies associated with chronic hepatitis and their clinical manifestations. Patients and method: Ninety anti-HCV-positive patients were consecutively interviewed and examined by the same operator. Forty-five patients with end-stage liver disease and awaiting liver transplantation were evaluated at the Liver Transplantation Center (Group 1). Further 45 patients were referred for neurological consultation during hospitalisation in the Department of Medicine (Group 2), where they had been admitted for different clinical reasons. One patient from group 1 and 5 patients from group 2 were excluded from the study because of previous neurological diseases. All patients underwent a standardized neurological evaluation, including history, neurological examination, mini mental state examination, neuropathy symptom score, and neurological disability score. In presence of symptoms and signs of peripheral neuropathy, an electrophysiological evaluation was performed. Results: Signs or history of encephalopathy were found in 23/44 patients of group 1 (52.2%) and in 8/40 patients of group 2 (20%). Clinical manifestations of neuropathy, confirmed by electrophysiological examination, were found in 11 subjects of group 1 (25%) and in 17 patients of group 2 (42.5%). Most patients had minor symptoms; sensory disturbances occurred more frequently than motor and autonomic dysfunctions. In group 1, peripheral neuropathy was associated with systemic illness (diabetes, renal failure, liver neoplasm, previous alcohol abuse) in 4/11 patients (36.3%); conversely, in all patients from group 2, other possible etiological factors were present: alcohol abuse in 3; diabetes in 4; renal failure in 1; mixed cryoglobulinemia in 7; and neoplasm in 2. Conclusions: Symptomatic but not disabling neuropathies were found in 33% of HCV in patients. Sensory involvement was prevalent. Systemic illness and mixed cryoglobulinemia were more frequently present in Group 2 than in Group 1. This finding suggests that the metabolic dysfunctions caused by liver disease may be the primary determinant of peripheral system damage only in patients with end-stage liver disease.

Epilepsy is a rare but possible manifestation of thyrotoxicosis. The patient reported here developed recurrent, generalized and focal seizures, as presenting symptoms of a thyrotoxic encephalopathy. Intercritic EEG records showed triphasic waves. Seizures and signs of encephalopathy disappeared and the EEG reverted to normal only after treatment of the thyroid hyperfunction. It is concluded that thyroid function should be evaluated in cases of otherwise unexplained encephalopathy with untreatable seizures and triphasic waves.