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Biomedical subjects

V Laulumaa

Publications and source records attributed to V Laulumaa.

23 records · Page 2Linked to original sources
PubMed1988

Peripheral neuropathy in late onset spinocerebellar ataxia.

We studied 10 patients with late onset spinocerebellar ataxia including electrophysiological and muscle biopsy examinations. Nerve conduction studies of eight patients revealed axonal neuropathy, and six cases also showed signs of the involvement of the lower motor neuron. In 9 patients quantitative analysis of single motor unit potentials (MUPs) of the tibialis anterior or biceps brachii muscles showed mild to severe neuropathic changes and in all 10 patients the histopathological examination of the tibialis anterior showed mild to severe neuropathic changes. Neither nerve conduction studies, quantitative MUP analysis, nor histological findings of the muscle were related to the severity of duration of the disease.

Biopsy↗
PubMed1987

Involvement of somatosensory and visual pathways in late onset ataxia.

Nerve conduction studies, median nerve somatosensory (SEPs) and pattern-reversal visual evoked potentials (VEPs) were recorded in 10 patients with late onset ataxia. Nine patients had dysfunction of somatosensory pathways, eight of them axonal polyneuropathy in nerve conduction measurements, and four had also impaired impulse conduction along the visual pathways. Abnormalities in records of evoked potentials occurred as prolonged latencies rather than reduced amplitudes. The observed dysfunction of peripheral and central pathways was not related to the duration or the severity of the clinical involvement by the disease. It is emphasized, however, that there seemed to be a relationship between the prolonged SEP latencies and the impaired peripheral nerve conduction values and between the diminished VEP amplitudes and the most delayed VEP latencies.

Adult↗
PubMed1987

Recent progress in the research of Alzheimer's disease.

The purpose of this review is to survey some of the recent advances made in the understanding of the basic mechanisms underlying cognitive functions and dysfunctions in Alzheimer's disease (AD). Cholinergic projections from the nucleus basalis of Meynert (nbM), which are involved in AD, have been related to certain memory functions. Information processing, attention or arousal may, however, be influenced by nbM neurons more than primary memory mechanisms. Perforant pathway and subiculum projections, which presumably use glutamate as a neurotransmitter, are involved in AD leading to the disconnection of the hippocampus from the neocortical areas. The hippocampus and entorhinal cortex seem to play an important role in learning and memory. The hippocampus can be regarded as a relay station for the processing of recent episodic memory, but information is bound to memory storage in the cortical association areas. An important finding has been the plasticity changes in the hippocampus seen after the destruction of entorhinal cortex. Antemortem markers of AD have been under extensive study. Alz-50 antigen may be one of the most promising findings in this area, but no definite biological marker of AD currently exists. A medication for treatment of AD is also under development.

Acetylcholine↗
PubMed1986

Somatostatin-like immunoreactivity in the cerebrospinal fluid of patients with Parkinson's disease and its relation to dementia.

Acetylcholinesterase, somatostatin-like immunoreactivity, and homovanillic acid levels were measured in the cerebrospinal fluid of 36 patients with early stages of Parkinson's disease and in 19 control patients. In patients with Parkinson's disease the levels of somatostatin-like immunoreactivity were lower than in the controls (p less than 0.01); these values were lowest in the demented Parkinsonian patients. Concentrations of homovanillic acid were also significantly lower in Parkinsonian patients (p less than 0.05). In contrast, no changes were observed in the acetylcholinesterase activity of patients with Parkinson's disease. The reduced somatostatin-like immunoreactivity in CSF agrees with previous post-mortem studies and indicates that Parkinson's disease and Alzheimer's disease may have some neurochemical features in common.

Acetylcholinesterase↗