ABSTRACT
Different clinical criteria for diagnosing dementia were compared in a sample of 69 patients with motor neurone disease (MND). Participants' performances on a computerised battery of neuropsychological tests were evaluated to assess the usefulness of these tests in predicting dementia in MND. The results indicated that when diagnostic criteria for frontotemporal (FTD) were used as part of a questionnaire method of diagnosing dementia the incidence of dementia in MND was considerably greater than traditional estimates suggest. Through a series of logistic and multiple regressions the results demonstrated that neuropsychological test performance related well to diagnostic classifications of dementia. MND patients with a clinical diagnosis of dementia were likely to demonstrate impaired new learning; poor working memory and planning; slowness in information processing and rigidity in thinking. These features, which are typical of cases of FTD, suggest that the dementia of MND is usefully characterised as a form of FTD. The finding that neuropsychological impairment correlated with behavioural features of dysexecutive impairment in daily living, indicates that the management focus in MND must be broadened to include cognitive/behavioural issues.
Subject(s)
Dementia/etiology , Dementia/psychology , Motor Neuron Disease/complications , Motor Neuron Disease/psychology , Severity of Illness Index , Adult , Aged , Aged, 80 and over , Dementia/diagnosis , Female , Humans , Male , Middle Aged , Neuropsychological Tests , Regression AnalysisABSTRACT
We have studied the pelvic floor musculature and its innervation in 14 of 24 (58 per cent) multiparous women who had been recruited into a study of the effect of childbirth on the pelvic floor as part of a prospective investigation that began in 1983. These 24 women had all delivered by the vaginal route without forceps assistance. Five of the 14 had developed clinical symptoms of stress incontinence 5 years later; two of them had had a further uncomplicated vaginal delivery during this time. There was manometric and neurophysiological evidence of weakness because of partial denervation of the pelvic floor striated sphincter musculature, with pudendal neuropathy, which was more marked in those women with incontinence. These findings provide direct evidence for the hypothesis that pudendal neuropathy due to vaginal delivery persists and may worsen with time.
Subject(s)
Delivery, Obstetric , Labor, Obstetric , Pelvis/physiopathology , Puerperal Disorders/etiology , Adult , Anal Canal/physiopathology , Female , Follow-Up Studies , Genitalia, Female/innervation , Humans , Motor Neurons/physiology , Muscle Contraction/physiology , Muscles/innervation , Nervous System Diseases/etiology , Parity , Pregnancy , Pressure , Prospective Studies , Urinary Incontinence, Stress/etiology , VaginaABSTRACT
The central and peripheral motor pathways serving striated sphincter muscle function were studied using cortical and lumbar transcutaneous electrical stimulation, pudendal nerve stimulation and sphincter electromyography in 23 patients with multiple sclerosis (MS), and sphincter disturbance, including incontinence of urine or faeces, urinary voiding dysfunction, or constipation. The central motor conduction time was significantly increased in the MS group compared to controls (p less than 0.05). Damage to both the upper and lower motor neuron pathways can contribute to sphincter disturbance in MS. The latter may be due to coexisting pathology or to involvement of the conus medullaris by MS.
Subject(s)
Anal Canal/innervation , Constipation/physiopathology , Fecal Incontinence/physiopathology , Motor Neurons/physiology , Pyramidal Tracts/physiopathology , Urethra/innervation , Urinary Bladder, Neurogenic/physiopathology , Adult , Cauda Equina/physiopathology , Electric Stimulation , Electromyography , Female , Humans , Male , Motor Cortex/physiopathology , Reaction Time/physiology , Synaptic Transmission/physiologyABSTRACT
Striated anal sphincter function was studied electrophysiologically and radiologically in six patients with Parkinson's disease and chronic constipation. In five cases, there was paradoxic anal sphincter muscle contraction during simulated defecation straining resembling anismus-type pelvic outlet obstruction. Radiologic studies showed functional improvement of the defecatory mechanism following the administration of the dopamine receptor agonist apomorphine in four patients. Dysfunction of the striated anal sphincter musculature may be a significant cause of constipation in some parkinsonian patients, occurring as part of the generalized extrapyramidal motor disorder.
Subject(s)
Anal Canal/physiopathology , Constipation/etiology , Parkinson Disease/physiopathology , Defecation/physiology , Electromyography , Female , Fluoroscopy/methods , Humans , Male , Middle Aged , Parkinson Disease/complicationsABSTRACT
Anismus, or constipation due to functional obstruction at the pelvic outlet by paradoxical contraction of the striated sphincter muscles during defaecation straining, is described in ten constipated patients and four patients with Parkinson's disease and constipation. The dysfunctional pattern of muscle recruitment resembled that characteristic of dystonia elsewhere in the body and was indistinguishable in patients with idiopathic anismus and those with extrapyramidal motor disturbance due to Parkinson's disease. These findings suggest that anismus may be a focal dystonic phenomenon.
Subject(s)
Constipation/physiopathology , Dystonia/physiopathology , Muscle Contraction , Parkinson Disease/physiopathology , Rectum/physiopathology , Adult , Aged , Anal Canal/physiopathology , Electromyography , Female , Humans , Male , Middle AgedABSTRACT
Binswanger, in his 1894 dissertation on the differential diagnosis of general paresis of the insane, described a slowly progressive dementia associated with macroscopic loss of white matter. In recent years interest in Binswanger's disease was rekindled with CT demonstration of extensive white matter low densities in some patients. To define the clinical spectrum, we reviewed 22 consecutive cases in which the CT appearances suggested a diagnosis of Binswanger's disease. Two patients had focal neurological deficits at presentation, but recent anoxic or hypoglycaemic insults could not be excluded as the cause of the CT abnormalities. The 20 remaining patients were demented and showed variable combinations of corticobulbar dysfunction and gait dyspraxia. The duration of symptoms ranged from a few months to several years. Sixty per cent of this group gave a history of discrete stroke events and focal cortical and/or lacunar infarcts were a frequent CT finding. Binswanger's disease is probably due to chronic or acute-on-chronic white matter ischaemia. The association with lacunar and cortical infarctions suggests that a combination of large and small vessel disease produces diffuse ischaemia maximal in white matter watershed zones. Binswanger's disease is clinically differentiated from multi-infarct dementia by its time course.