Transient global amnesia

can be recommended strongly to anyone interested in the modern treatment of neoplastic diseases. This monograph presents a discussion of the current concepts of clinical and pathological classification of Hodgkin's disease, approaches to therapy and clinical management. Among the advantages of the presentation are the excellent compilations of the classifications of the disease and tabulations of results achieved to date with regard to therapy and survival. While the author has carefully reviewed the pertinent material, his comments and conclusions are inexplicable in many instances. Examples include the recommendation for radical surgery in early or focal disease. None of the surgical series is a randomized prospective study nor do the majority include an adequate number of cases for statistical validity to warrant the author's recommendation. In presenting Kaplan's results with radical radio-therapy, there is an excellent reproduction of data showing the superiority of radical versus conventional radiotherapy. The author comments nevertheless that conventional therapy is \"fairly satisfactory !\" The scheme for radiotherapy of Stage I is reasonable, but the method employed is not that of most centers utilizing the radical approach in this country. For Stage III disease the plan seems less comprehensible since it involves treatment of involved but not adjacent areas. If it is intended to be \"curative,\" there is inadequate therapy for adjacent areas. If it is intended to be palliative, it would be unnecessary to treat asymptomatic although involved areas. The discussion of chemotherapy consists of general comments regarding efficacy and toxicity without a well defined analysis of comparative responses derived from objective assessment. A few opinions are cited without data to support the claims. In presenting clinical problems in the management of the disease, there are references to the immunological studies of patients with Hodgkin's disease, but no description of the specific immunologic status. Extra-nodal Hodgkin's disease as a specific entity also appears to have been neglected. In summary, this monograph provides an interesting review of some advances in Hodgkin's disease. The quality of the presentation in terms of organization and conclusions could be improved. The diagnosis and proper understanding of neurologic disorders depend heavily on thorough knowledge of the structure of the nervous system, and of the relationships between structure and function. Dr. Brodal's work represents an authoritative exposition of these relationships. The present edition is a thorough revision of the original book, published in English in 1946. Comparison of the two volumes provides a …

Neurological Anatomy in Relation to Clinical Medicine

Microbubbles : Pathophysiology and clinical implications

In divers, the significance of a patent foramen ovale and its potential relation to paradoxical gas emboli remain uncertain This study found that regardless of whether a diver has a patent foramen

/pdf/relation-between-directly-detected-patent-foramen-ovale-and-2czxxi60tl.pdf

Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2005.089862

A single air dive reduces arterial endothelial function in man

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.

https://oem.bmj.com/content/oemed/48/4/258.full.pdf

Neurological long term consequences of deep diving.

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.

https://oem.bmj.com/content/oemed/47/10/708.full.pdf

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

Neurological signs andsymptomswererecordedfrom156airandsaturation divers and100 controls. Fifty one(33%) ofthedivers hadhad symptomsfromthecentral nervoussystem during decompression. Also, 22(14%)hadbeen unconscious whilediving. Intotal 79(51%)had had decompression sickness (DCS).Twelve (8%)ofthediversandno controls hadhad specific neurological symptoms(vision disturbances, vertigo, reducedskinsensitivity) in non-diving situations, and six(4%)ofthe divers(nocontrols) had had episodes of cerebraldysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divershadsignificantly more general symptoms from thenervoussystemand more abnormalneurological findings thanthecontrols. The most prominent symptomswere difficulties in concentration and problems withlongandshorttermmemory.Themost prominentabnormalfindings inthedivers werecompatible withdysfunction inthedistal spinal cordor nerveroots,andpolyneuropathy.The generalneurological symptoms andfindings wereindependently significantly correlated withdiving exposure, prevalence of DCS,andage.

Influence ofoccupational diving upon thenervous system:an epidemiological study

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

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. Language: en

B K Kambestad

Papers

Neurological long term consequences of deep diving.

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

Influence ofoccupational diving upon thenervous system:an epidemiological study

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

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