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Biomedical subjects

K Arasaki

Publications and source records attributed to K Arasaki.

26 records · Page 2Linked to original sources
PubMed1989

Maximal and minimal motor nerve conduction velocities in amyotrophic lateral sclerosis.

In 15 patients with amyotrophic lateral sclerosis (ALS) and 20 age-matched control subjects, we measured the maximal and minimal motor nerve conduction velocities of the ulnar nerve as well as the action potential amplitude of the abductor digiti minimi muscle. Both maximal and minimal motor nerve conduction velocities in ALS patients were significantly lower than those in the control group. However, the difference between the maximal and minimal conduction velocities in each ALS patient was not statistically different from that in each control subject. The maximal action potential amplitude of the muscle in the ALS patients was significantly smaller than that in the control group.

Adult↗
PubMed1989

[Disorders of the nervous system associated with the acquired immunodeficiency syndrome (AIDS)-clinical approach].

The acquired immunodeficiency syndrome (AIDS) is caused by human immunodeficiency virus (HIV) and characterized by disorders of the nervous system in addition to opportunistic infection and cancer. Centers for Disease Control (CDC) recommend the classification system consisting of four major groups. Group I is patients with acute HIV infection, and Group II is asymptomatic carriers. Group III is those with persistent generalized lymphadenopathy (PGL). Group IV includes five subgroups: IVA with constitutional disease, IVB with neurologic disease, IVC with secondary infectious diseases, IVD with secondary cancers and IVE with other conditions. The nervous system disorders are classified into two types: one is produced by HIV itself and not directly related to immunodeficiency, and the other caused by opportunistic infectious agents and cancers. The former is further divided into two kinds: atypical aseptic meningitis and acute inflammatory demyelinating polyneuropathy (AIDP) occur mainly in Group I and II, whereas HIV encephalopathy, distal symmetric polyneuropathy (DSPN) and vacuolar myelopathy in Group III and IV. Group I or II patients have no apparent medical problems. Therefore, when neurologists see patients with risk factors for HIV infection presenting with atypical meningitis or AIDP, it is of utmost importance to have a high index of suspicion and to look for evidence of HIV infection.

AIDS Dementia Complex↗
PubMed1987

Limbic lymphoma.

Two cases of metastatic malignant lymphoma confined to the limbic-hypothalamic region are presented. The non-specific nature of the neurological symptoms associated with these lesions such as memory loss, impotence and confusion made neurological localization of the disease process difficult. While non-contrast computed tomography (CT) was unremarkable, contrast CT was diagnostic, showing bilateral homogenous enhancement of specific limbic-hypothalamic structures without significant mass effect. Since lymphomatous involvement of the limbic-hypothalamic area tends to be infiltrative without attendant mass effect, detection of metastasis may be elusive unless special attention is directed to this region. As lymphoma is often chemoresponsive and highly radiosensitive, early recognition of limbic-hypothalamic involvement of this disease is important.

Hodgkin Disease↗
PubMed1984

Firing of spinal motoneurones due to electrical interaction in the rat: an in vitro study.

The excitatory interaction between spinal motoneurones was investigated by means of electromyogram (EMG) recordings from hindlimb muscles as well as intracellular ones from their innervating motoneurones in the isolated preparation of immature rats. Stimulation of the muscle nerve to biceps femoris or medial gastrocnemius or of the L5 ventral root evoked early and late EMG responses in the muscle of the preparations with the dorsal roots cut. The early response was produced directly by volleys in the motor nerve. The late response was of spinal origin, since it disappeared after the severance of the ventral root. The thresholds and the conduction velocities of nerve fibres, which conducted the centripetal impulse causing the late response, were compatible with those of motor nerve fibres. The amplitude of the late response was 5-10% of that of the maximum early EMG response. Intracellular recordings from spinal motoneurones revealed that stimulation of the ventral root elicited the double discharge composed of antidromic and delayed spike potentials. The delayed spike was never evoked after the spike potential elicited directly by a short depolarizing pulse. The double discharge was observed in about 6% of the motoneurones examined. The threshold of the stimulus intensity evoking the double discharge was in the range of those of motor nerve fibres. The latencies of the delayed excitation were 7.0-9.0 ms, comparable to the intraspinal delays of the late EMG response. Stimulation of the ventral root at intensities subthreshold for antidromic activation was found to produce a small depolarizing potential in about 60% of the motoneurones examined. The amplitudes were 0.5-5.0 mV, and the onset and the peak latencies 2.0-7.0 ms and 5.0-8.0 ms, respectively. The potential was unaffected by the deficiency of calcium ions in the perfusing medium and persisted after the degeneration of the afferent fibres in the ventral root.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1983

Origins of short latency somatosensory evoked potentials to median nerve stimulation.

Short latency SEPs recorded in hand-scalp, ear-scalp and upper neck-scalp leads with stimulation of the median nerve were examined in 27 normal subjects and in 11 selected patients with unilateral complete loss of position sense in order to provide information concerning the generator sources of these potentials. Evidences obtained from both normal subjects and patients suggest the following origins for these short latency SEPs. In hand reference recording, P1 may arise in the brachial plexus just beneath the clavicle, P2 in the cervical dorsal column, P3 mainly in the caudal brain stem, and P4 primarily in the brain stem lemniscal pathways and partly in the thalamus. The initial negative potential recorded in upper neck-scalp leads may originate largely in the cervical dorsal columns. The early positive potential recorded in ear-scalp leads may reflect activity mainly in the brain stem lemniscal pathways and partly in the thalamus. The initial negative component of the cortical SEPs (N1) may arise in the thalamus, and the subsequent positive component (P1) may reflect activity in the primary somatosensory cortex.

Adult↗
PubMed1982

Origins of the scalp-recorded somatosensory far field potentials in man and cat.

Short latency somatosensory evoked potentials preceding the primary cortical potential were recorded from the scalp in man and cats. Four positive potentials (P1, P2, P3 and P4 in man, and CI, CII, CIII and CIV in cats) were observed with non-cephalic reference recording and 3 or 2 positive components (P1a, P2a and P3a in man, and CIa and CIIa in cats) were recorded with earlobe reference. (1) The latencies of these potentials and the effects of lesions on them in man and (2) the effects of (i) supracollicular and medullo-cervical transections and (ii) intrathecal anaesthesia of the cervical cord on these components in cats suggest that: (1) P1 and CI originate in the brachial plexus beneath the clavicle; (2) P2, P3 and CII, CIII are generated in the cervical cord; (3) P4 and CIV reflect activity mainly in the brain stem or the cerebellum or both; (4) P1a and CIa arise in the cervical cord; (5) P3a and CIIa reflect activity mainly in the brain stem or the cerebellum or both. As the impulse initiated in the median nerve travels through various regions where the resistance might change suddenly, these far field potentials might be recorded as if generated at fixed sites such as just beneath the clavicle and foramen magnum.

Animals↗