Severity Of Neurological Impairment Research Articles

Olfactory loss in multiple sclerosis.

The objectives of the present study were to test odor identification ability in patients with multiple sclerosis (MS) and to examine possible correlations between smell identification test scores and various clinical variables. We performed a case-control study comparing the Cross Cultural Smell Identification Test scores of 40 patients with definite multiple sclerosis with those obtained in 40 age-, sex- and smoking-habit-matched healthy controls. The neurological impairment, the disability, the cognitive performances and the psychological functioning were also assessed. Patients with multiple sclerosis scored significantly poorer than controls on the Cross-Cultural Smell Identification Test (P<0.001). Olfactory function was borderline normal in four (10%) and abnormal in five (12.5%) MS patients, whereas it was normal in all controls (P<0.02). Significant correlations between the smell identification score and symptoms of anxiety (r=-0.43, P=0.006), depression (r=-0.42, P=0. 008) and severity of neurological impairment (r=-0.32, P=0.05) were found. Only two (5%) patients with multiple sclerosis reported having episodes of smell loss, suggesting a low level of awareness of this problem. Although smell changes are rarely reported, olfactory function is impaired in a considerable number of patients with MS. The observed association between decreased odor identification ability and symptoms of anxiety and depression in our patients suggests that mood and anxiety disorders have to be considered in assessing olfaction in MS patients. Clearly, smell disturbances deserve greater attention from health professionals and caregivers dealing with such patients.

Neuropsychological Profile Associated with Silicone-gel Breast Implants

Thirty-two silicone breast implant patients scored in the mild to moderate range of impairment on the Halstead-Reitan Neuropsychological Battery. An unusual number of patients had positive tests for antinuclear antibody on immunological testing and a high incidence of electroencephalogram (EEG) abnormalities were found. Personality testing revealed a Minnesota Multiphasic Personality Inventory (MMPI) profile which is found in neuropsychologically impaired subjects, but which is also consistent with extreme emotional distress that may result in somatic complaints. None of the subjects was near the cut-off score for malingering or faking bad on the F- K index of the MMPI. There was no apparent relationship between length of exposure and the severity of neurological impairment. In addition, the performance of explanted subjects was not improved when compared to subjects whose implants were still in place.

Selective increases of extracellular brain concentrations of aromatic and branched-chain amino acids in relation to deterioration of neurological status in acute (ischemic) liver failure.

Previous reports based on studies in brain tissue from humans and experimental animals suggest that aromatic amino acids (AAAs) and branched-chain amino acids (BCAA's) accumulate in brain in acute liver failure. In order to assess these changes in relation to the severity of neurological impairment and to the degree of hyperammonemia, AAAs and BCAAs were measured in vivo by cerebral microdialysis in frontal cortex of rats at various stages during the development of hepatic encephalopathy due to acute liver failure resulting from portacaval anastomosis followed by hepatic artery ligation. Extracellular brain concentrations of AAAs and of valine and leucine were elevated 2 to 4-fold following hepatic devascularization and these increases were significantly correlated to arterial ammonia concentration (r= 0.71-0.84, p<0.05). Extracellular concentrations of tyrosine paralleled the deterioration of neurological status in acute liver failure rats. In view of their role as precursors of monoamine neurotransmitters, ammonia-induced alterations of intracellular/extracellular brain concentration ratios for AAAs could account for altered neuronal excitability and contribute to the encephalopathy characteristic of acute liver failure.

Reversible ischemia increases levels of Alzheimer amyloid protein precursor without increasing levels of mRNA in the rabbit spinal cord

In a rabbit spinal cord ischemia model (RSCIM), the time courses of neuropathological damage of the spinal cord and neurological impairment of the motor functions are well established, demonstrating that the extent of neuropathological damage and the severity of neurological impairment are closely correlated. We used the RSCIM to elucidate the effects of reversible (15 min) and irreversible (60 min) ischemia on the endogenous levels of amyloid protein precursors (APPs) at both the mRNA and protein levels in the caudolumbar/sacral region of the spinal cord. We speculate that endogenous APPs are induced by ischemia as either trophic factors or stress-induced proteins in the RSCIM. A 15-min occlusion transiently increased the APP protein levels in neurons, which returned to the original levels by the end of 60 min occlusion. The increase in APP protein levels during 15-min ischemic insult does not appear to involve regulation at the mRNA level. The increased level of APPs, particularly of the soluble form, could support the possibility that APPs play a neuroprotective role in the RSCIM as stress-induced proteins. In contrast, failure to maintain the increased APP protein levels or to increase the mRNA, as seen in the 60-min ischemia samples, may be one of the causal factors that induce necrosis and neuronal cell death leading to irreversible neurological impairment.

Psychosocial and neurological predictors of mental health in multiple sclerosis patients

Multiple Sclerosis (MS) is a chronic and unpredictable disease, largely uncontrolled by current treatment. Its effects vary from a mild course with minimal disabilities to a rapidly progressing or fluctuating course with devastating disabilities. No reliable indicators exist to assure patients that their status will remain stable or that disabilities will not emerge or progress. Furthermore, patients confront symptoms that frequently and unpredictably vary with respect to form and intensity, sometimes daily. Over the short and long term, the unpredictability and mutability of MS-related disabilities pose particular adjustment problems. For these reasons, there has been increasing interest in studying psychosocial adjustment in MS patients. Unfortunately, many studies of adjustment have suffered from methodological flaws (see, for review, Devins and Seland [l]). In particular, several studies fail to take adequate account of physiological disease factors in the assessment of psychological status. Assessment instruments have been employed that misclassify somatic complaints, often reflecting neurological dysfunction in MS, as evidence of psychopathology. The Minnesota Multiphasic Personality Inventory (MMPI) [2] and General Health Questionnaire (GHQ) [3] are examples of inventories that misclassify neurological impairment in this way, likely overestimating the prevalence of mood and personality disorders in MS patients [4,5]. Certainly, accounting for the effects of physical symptoms on psychological status is of major importance in evaluating factors affecting adjustment. Thus, the search for predictive factors requires multifactorial designs, evaluating theoretically cohesive models of adequately measured physical and psychosocial factors. In this study, we investigated a model that included disease status, physical disability, and psychosocial measures to identify key factors affecting the mental health of MS patients. Our goal was a model of factors that could guide intervention programs assisting psychosocial adjustment. We conceptualized five sets of factors: neurological impairment, disease duration, physical disability, disease-related symptoms, and psychosocial factors. In further specifying variables, in terms of neurological impairment, we considered both the current severity of neurological impairment and the duration of disease (measured from the onset of disease perceived by the patient) as potentially significant contributors to mental health status. Physical disability indices were used to assess whether the sickness-related disruption of physical functioning, affecting ambulation, mobility, and body care, would have

Motor recovery after stroke. Morphological and functional brain alterations.

The aim of this study was to evaluate the relationships of morphological and CBF patterns with both the severity and the evolution of the motor deficit in the late phase of stroke and, in particular, to identify morphological and/or functional brain alterations associated with a persistent severe motor deficit or a poor, delayed motor recovery. We analysed CT/MRI and single photon emission tomography (SPET) findings from 37 patients studied in the chronic phase of stroke (mean duration +/- SD = 3.6 +/- 1.6 months), whom we were able to follow clinically for a period of 3 months. The eventual degree of motor recovery correlated significantly (negatively) with the time since stroke at entry, but not with the severity of neurological impairment at entry. The volume, side and location (cortical or subcortical) of the infarct did not correlate with either the severity or the evolution of the motor deficit. Patients with a CT/MRI lesion of the parietal lobe (n = 8) showed a more severe motor deficit than those with other cortical locations. The severity of the motor deficit correlated significantly (negatively) with CBF values in the supplementary motor area (SMA) and parietal areas of the damaged hemisphere, and in the contralateral undamaged primary motor cortex. The degree of motor improvement correlated significantly (positively) with CBF values in the contralateral undamaged thalamus, lentiform and caudate nuclei, and premotor cortex. In the late phase of stroke, the severity of the motor deficit may be positively associated with the functional impairment of associative parietal and frontal areas of the damaged hemisphere. The functional impairment of the basal ganglia-frontal network in the undamaged hemisphere seems to be related to a poor, delayed motor recovery.

Clinical definition for multiple sclerosis treatment trials

Clinically, the Schumacher Panel criteria remain the best set of diagnostic criteria. Two subsets therein are definable, i.e., exacerbating-remitting (ER) and chronic progressive (CP), with the latter subdivided into progressive from onset and secondarily progressive. A clinically stable stage can also be recognized. It has been customary in treatment trials to separate ER and CP patients. End point for the latter is a comparison of neurologic status at the end of the trial with that entry. A similar assessment can be made for ER patients. With this criterion both types could be included in a single study. One could also, though, treat the exacerbation in an acute study or assess whether exacerbations can be prevented in a long-term trial. Most clinicians no longer consider monophasic disease as multiple sclerosis (MS). Depending on clinical extent, such patients are divisible into acute disseminated encephalomyelitis, Devic disease, transverse myelopathy, or optic neuritis. Each subgroup could be studied as with an acute exacerbation or in long term as to whether future and different neurologic insults can be prevented. One measure of neurologic status is the Disability Status Scale (DSS), which grades clinical impairment due to MS on a 0 (normal) to 10 (death due to MS) basis. The expanded DSS (EDSS) subdivides each step 1 through 9 into two. Type and severity of neurologic impairment is defined by graded involvement in the following eight functional systems (FS): pyramidal, cerebellar, brainstem, sensory, bowel and bladder, visual, cerebral, and other. Frequency and severity of each FS correlates strongly with DSS scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain imaging in late-onset GM2 gangliosidosis.

We describe brain CT and MRI characteristics of 10 patients with late-onset GM2 gangliosidosis. Cerebellar atrophy, particularly of the vermis, was a prominent feature in all patients with normal-appearing cerebral hemispheres. The severity of these findings did not correlate with the age of onset, disease duration, severity of neurologic impairment, or mode and distribution of the various clinical presentations. In particular, no cerebral abnormality was found by neuroimaging in seven patients with intellectual decline and in six patients with recurrent psychosis, while prominent cerebellar atrophy was present in the only patient who was free of cerebellar signs.

HEMIPLEGIC CEREBRAL PALSY

Morphological findings on CT were compared with clinical features of 111 children with hemiplegic cerebral palsy. Periventricular atrophy, interpreted as periventricular leukomalacia, was the most prevalent CT finding, although this type of lesion did not indicate severity of neurological impairment. Maldevelopments were associated with arm-dominated hemiplegia and with a wider range of clinical impairments than previously described. Cortical/subcortical atrophy, less common than presumed, indicated arm-dominated hemiplegia and was associated with more severe impairment than were other CT findings. A normal CT scan indicated leg-dominated hemiplegia and mild impairment. The morphological information obtained by CT was found to be useful for predicting clinical outcome, and was considered an important adjunct to clinical history and findings in these children.

Neurological and neuropsychiatric spectrum of Wilson's disease: a prospective study of 45 cases

Forty-five patients with Wilson's disease (WD) were prospectively studied: 27 had neurological deficits, 12 hepatic signs, and 6 were asymptomatic. Kayser-Fleischer rings occurred in 23 of the neurological patients and in only 4 of the hepatic patients. Neurological features were extremely variable with respect to frequency and severity. Most frequent were dysdiadochokinesis (25 patients), dysarthria (23), bradykinesia (17), and posture tremor (14). Fifteen, mainly long-term treated patients, presented with rather discrete neurological abnormalities which predominantly consisted of dysarthria and various forms of tremor. Eight patients had a parkinsonian type of neurological WD associated with signs of an organic mood syndrome. Three patients were predominantly hyperkinetic, presenting with dystonic and choreatic movements. In 1 patient, ataxia was the predominant neurological feature. There was a clear-cut correlation between the severity of neurological impairment and the restriction in functional capacity. Nine patients were not able to engage in salaried employment or were retired. Psychiatric symptoms and behavioural disorders were common, varying from mild personality and psychological disturbances to severe psychiatric illness resembling psychotic disorders and major depressive syndromes. Significant mental deterioration was not found in the patients. Disturbances of mood were observed in 12 patients, all of whom had neurological abnormalities. There was a history of an attempted suicide in 7 patients, and a history of an organic delusional syndrome in 3.

Hemiplegic Cerebral Palsy: Correlation Between Ct Morphology and Clinical Findings

Morphological findings on CT were compared with clinical features of 111 children with hemiplegic cerebral palsy. Periventricular atrophy, interpreted as periventricular leukomalacia, was the most prevalent CT finding, although this type of lesion did not indicate severity of neurological impairment. Maldevelopments were associated with arm-dominated hemiplegia and with a wider range of clinical impairments than previously described. Cortical/subcortical atrophy, less common than presumed, indicated arm-dominated hemiplegia and was associated with more severe impairment than were other CT findings. A normal CT scan indicated leg-dominated hemiplegia and mild impairment. The morphological information obtained by CT was found to be useful for predicting clinical outcome, and was considered an important adjunct to clinical history and findings in these children.