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Biomedical subjects

K Todnem

Publications and source records attributed to K Todnem.

14 recordsLinked to original sources

[Neurological decompression sickness].

We have examined 34 divers, mean age 30 years, after treatment for neurological decompression sickness. The initial symptoms often indicated mild sensory or motor involvement. After recompression treatment five of 19 divers with primary affection of the brain had slight hemiparesis or dysphasia. Nine of 14 divers with primary affection of the spinal cord showed signs of spinal cord dysfunction following treatment. Only 16 divers were recompressed within six hours after start of the neurological symptoms. It is concluded that neurological decompression sickness is a serious disorder with a high rate of residual findings. The condition should be treated with prompt recompression, administration of oxygen, and intravenous fluid.

Adult

Electroencephalography, evoked potentials and MRI brain scans in saturation divers. An epidemiological study.

One hundred and fifty-six air and saturation divers, mean age 33.6 (range 21-49) years, were examined. The control group consisted of 100 offshore workers and policemen with the health requirements to have a diving certificate, mean age 34.0 (range 22-48) years. The examination protocol included electroencephalography (EEG), visual evoked potentials (VEPs), brain-stem auditory evoked potentials (BAEPs) and magnetic resonance imaging (MRI) of the brain and brain-stem. Abnormal EEGs, with focal slow waves mostly in the temporal regions and sharp potentials, were found in 18% of the divers and in 5% of the controls (P = 0.003). Abnormal EEGs correlated significantly with the exposure to saturation diving (P = 0.0006) and the prevalence of decompression sickness (P = 0.0102). Alcohol consumption was negatively correlated with abnormal EEGs (P = 0.0006). Mean I-III BAEP latency was increased (P = 0.047) in the diver group. P100 VEP latency decreased with age (21-49 years). High signal intensity changes obtained by MRI were found in 33% of the divers and in 43% of the controls (P = 0.14). It is concluded that the nervous system of saturation divers is influenced by their occupation and that EEG is a useful method in the health examination of divers.

Adult

Neurological long term consequences of deep diving.

Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers.

Adult

Visual evoked and brain stem auditory evoked potentials in divers.

Visual evoked potentials (VEP) were examined in 14 divers during dives to 360 metres of seawater (msw). All latencies increased significantly with depth. VEP and brain stem auditory evoked potentials (BAEP) were similarly examined in 18 divers before and after these dives. N75 was significantly increased after compared to before the dive, while there was no significant difference in the P100 and N145 latencies. BAEP I-V latency was significantly decreased after the dives. VEP and BAEP were examined in 156 divers and 99 controls. There was no significant difference in VEP. BAEP I-III interpeak latency was significantly increased for the divers, but with no significant changes in I-V and III-V latencies. VEP and BAEP were examined in 26 divers after treatment for neurological decompression sickness. There was no significant difference compared to the control group. The conclusions are that VEP and BAEP change transitorily with influence of hyperbaric pressure, but do not measure major permanent disturbances in the divers' visual and auditory pathways.

Adult

Influence of occupational diving upon the nervous system: an epidemiological study.

Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.

Adult

Cerebellar lesion, polyneuropathy and mental dysfunction in a seaman working on chemical tankers.

A seaman with symptoms and signs from the nervous system was examined. He had symptoms and signs of affection of his mental status, cerebellum and peripheral nerves. He had been working on tankers for 31 years, and had regularly been exposed to different organic solvents during loading, unloading and cleaning of the tanks. As no other disease was present in this patient, the existence of a chronic organic solvent intoxication syndrome was suggested.

Cerebellum

Analysis of neurologic symptoms in deep diving: implications for selection of divers.

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.

Adult

Immediate neurological effects of diving to a depth of 360 metres.

Eighteen divers performed a simulated dive to a depth of 360 metres of seawater breathing a mixture of helium and oxygen. Clinical neurological examinations and neurophysiological tests were performed before and after the dives. Two divers had mild ataxic signs and changed electronystagmography after the dive, and one had impaired vibration sense in one lower extremity. Abnormal EEGs with slow waves and sharp potentials, seen primarily in the temporal regions, occurred in 2 divers. No changes were found in the magnetic resonance imaging brain scans. The divers with evidence of previous central nervous system injury, or a history of unconsciousness or previous decompression sickness seemed more likely to develop neurological signs after these deep dives. This study shows that deep diving may induce immediate neurological changes. We recommend that future deep divers have a neurological examination and 2 separate EEGs included in their medical examinations.

Adult

The non-linear relationship between nerve conduction velocity and skin temperature.

Median motor and sensory nerves were examined in 20 healthy subjects. Superficial stimulating and recording electrodes were used, and the nerves were examined at natural skin temperature, after cooling and after heating of the arm. The conduction velocity for the fastest and slow conducting sensory fibres (temperature range 17-37 degrees C), and for the fastest conducting motor fibres (temperature range 19-38 degrees C) increased non-linearly with increase in skin temperature. Similarly, distal motor latencies increased non-linearly with decrease in skin temperature. The effect of temperature was most pronounced in the low temperature range, and change in conduction velocity per degree centigrade was reduced toward higher skin temperature. Sensory nerve response duration increased linearly with decline in skin temperature. Sensory and motor amplitude did not show any significant relation to skin temperature.

Adult

Nerve conduction velocity in man during deep diving to 360 msw.

The function of the sensory and motor median nerves was examined in 6 divers during a simulated dive to 360 meters of seawater (msw), with a mixture of helium and oxygen (heliox) as breathing gas. Divers were examined in the compression chamber before the dive, at 360, 300, 240, 130, 50, and 5 msw, and with skin temperatures ranging from 29.2 degrees to 35.2 degrees C. Examinations were performed with superficial stimulating and recording electrodes. Fast sensory nerve conduction decreased with increase in hyperbaric pressure and with decrease in skin temperature. There was no significant correlation between slow sensory conduction and hyperbaric pressure. Distal motor latency increased with increase in hyperbaric pressure and with decrease in skin temperature. The effect of pressure was independent of temperature. No significant functional changes were detected in the main nerve trunk proximal to the wrist or in the F-wave responses.

Adult

Seamen exposed to organic solvents. A cross-sectional study with special reference to the nervous system.

A cross-sectional study of 85 long-term solvent exposed seamen working on chemical tankers compared to 59 unexposed seamen. Symptoms from the nervous system, clinical neurological findings and neurographic measurements were studied. The examinations were performed at least 2 weeks after the last solvent exposure. A stepwise multiple regression analysis was used to evaluate the dose-response relationship between the registered data on one hand and solvent exposure, employment on chemical tankers, age, alcohol and chloroquine phosphate consumption on the other. A significant correlation was found between increasing solvent exposure and reduced sensory nerve conduction velocities, as well as between increasing solvent exposure and prolonged distal latencies of motor nerves, and between increasing exposure and reduction of action potential amplitudes of sensory nerves. No correlation was found between solvent exposure and symptoms from the nervous system or clinical neurological findings.

Chloroquine

A patient with Cronkhite-Canada syndrome, myxedema and muscle atrophy.

A case of Cronkhite-Canada syndrome is presented. The patient had alopecia, onychodystrophy and gastrointestinal polyposis, mainly in the stomach and duodenum, with transient diarrhea and hypoproteinemia. Marked atrophy and weakness of the shoulder girdle muscles due to myopathy were also present. In addition she had primary hypothyroidism. The outcome of the disease is usually fatal within months, but so far our patient is alive four years after the onset of symptoms. The pathological changes, pathophysiology, symptoms, course and treatment of this rare disorder of unknown etiology are discussed.

Aged