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PubMedDate not supplied

[Semiologic aspects of traumatic coma (author's transl)].

After studying 85 patients with severe traumatic coma and reviewing the published literature, the authors propose a simple clinical procedure for the diagnostic of such cases. This classification is based on signs without any ambiguity, easily recognized by different physicians, and of pathognomonic significance. These include reaction to pain, testing four reflexes integrated at different levels in the brain stem, pupil morphology, and spontaneous ocular movements. The clinical features corresponding to different levels of dysfunction in the brain are described and their characteristics outlined. The importance of motor reactivity to pain associated to the brain stem reflexes (fronto-orbicular, photomotor, horizontal and vertical oculo-encephalic) is stressed.

Brain Stem↗
PubMedDate not supplied

[Severe traumatic coma from diffuse brain lesions (neuropathological aspects) (author's transl)].

From a review of recent literature, and pathological study of more than 100 personal cases, the authors describe the most interesting of these "diffuse" lesions; they only recall the most common types of lesions (contusions, vascular lesions, edema and its consequences - especially on brain stem); but a more detailed description is given of less known lesions of corpus callosum, brain stem and white matter, which have a more complex pathogeny (direct physical injury, anoxia-ischaemia, edema), and which they consider to be factors which worsen or protract the coma. "Biochemical" lesions (basic myelinic protein, liberated "false" neurotransmitters) are also discussed.

Brain↗
PubMedDate not supplied

[EEG in post-traumatic coma. Diagnostic and prognostic value (author's transl)].

This study concerns 1600 post-traumatic acute comas, who underwent combined clinical and EEG examinations. The EEG has been recorded accurately bedside several times a day throughout the acute stage. The obtained EEG patterns, generally considered to be polimorphous and extremely variable, can be classified into five basic groups corresponding to progressive deterioration of the cerebral electrogenesis: borderline, changeable, sleep-like, monotonous and silent. Borderline, sleep-like and changeable patterns, even though they indicate a varying degree of impairment of cerebral electrogenesis, prove nevertheless that the brain is capable of elaborating physiological rhythms and of modifying its activity in a spontaneous or evoked manner. True slow monotonous activity indicates an extreme degree of cerebral impairment; flattening, up to EEG silence, indicates the onset of brain death. Focal slowing and/or flattening, which often lacks surgical significance, is not considered in this classification. Focal or generalized irritative activity in the early stages, however, indicates a more severe condition. EEG has often proved to be an useful means supporting the diagnostic and prognostic value of clinical examination.

Brain↗
PubMedDate not supplied

[Post-traumatic coma from diffuse brain lesions. A correlative study of the levels of dysfunction and the EEG nyctohemeral aspects (author's transl)].

Thirteen EEG and polygraphic recordings were performed during a 24-hour period in 11 patients with post-traumatic coma. Spontaneous fluctuations, reactivity, and the organization of electrical activity were studied throughout the nyctohemeral period. The results were compared with the data obtained from clinical examinations evaluated in terms of the level of neurological dysfunction. The level of impairment of the EEG was usually a valid indication of the level of neurological dysfunction, the EEG results being sometimes more precise than the clinical data. In regard to the prognosis, the disappearance in the EEG of any fluctuations coincided with an unfavourable evolution.

Brain↗
PubMed1985

[Coma in full-term newborn infants following acute fetal distress: electro-clinical evolution].

Twenty full term infants who had birth asphyxia were studied. These infants were in a comatose state for 4 to 15 days and at least 3 EEG recordings were performed during this period. Six infants recovered without sequelae and in 2 cases there were minor abnormalities. In 7 cases there were major deficits (follow-up: 1 to 9 years) and 5 infants died within 15 days. Abnormal movements were observed in all the babies. Thirteen infants had EEG documented seizures (intermittent in 5 cases and status epilepticus in 8 cases). The prognosis was not correlated with the time of onset or duration of the coma, the time of onset or type of abnormal movements, nor with the presence of intermittent or continuous electrographic seizure activity. The initial tracing on the first day is the most significant prognostic factor. On subsequent days, an inactive EEG always indicated a poor prognosis. An improvement in the EEG on the 2nd on the 3rd day may not correlate with a favourable outcome since 3 such cases had a poor outcome. The clinical and EEG findings during therapy and the value of high levels of anticonvulsant therapy are discussed.

Coma↗
PubMed1998

Two chlorzoxazone (Parafon forte) overdoses and coma in one patient: reversal with flumazenil.

Chlorzoxazone (Parafon forte) overdose is rarely reported despite widespread use of this drug. This report describes a case of two episodes of chlorzoxazone overdose and coma in the same patient. Intubation and mechanical ventilation were required on the first presentation. Following the second overdose, intubation was averted and drug effects were reversed by use of the benzodiazepine antagonist, flumazenil. Although chlorzoxazone is not classified as a benzodiazepine, it may interact with benzodiazepine receptors, thus making flumazenil potentially useful in overdose states.

Antidotes↗
PubMed2001

[Febrile coma and multiple organ failure: suspected hemoglobinopathy SC].

We report the case of febrile fatal coma in a 51-year-old man from Burkina Faso. Magnetic resonance imaging (MRI) shows cerebral fat embolism. Haemoglobin electrophoresis shows probably haemoglobinopathy SC. A short review of the literature demonstrate the need to consider this complication in patients with neurological or respiratory disorders, in areas where this disease is highly prevalent, irrespective of age. It also emphasizes the diagnostic contribution of MRI and discusses the mechanism, the diagnosis as well as the difficulty of choosing the appropriate therapeutic course.

Anemia, Sickle Cell↗
PubMed1993

[Nosocomial Aeromonas hydrophila pneumonia complicating toxic coma].

A 24-year-old male homosexual drug addict was admitted in coma and circulatory failure after a 10 g overdose of acebutolol. The usual resuscitative measures were undertaken, together with administration of adrenaline and gastric lavage. Six hours of external cardiac massage and pacing, and high catecholamine doses (36 mg.h-1 of adrenaline and 60 micrograms.kg-1 x min-1 of dobutamine) were required before the circulatory system became again spontaneously efficient. After this acute episode, the patient improved despite acute tubular necrosis. On the third day, bilateral alveolar and interstitial lesions were found on the chest film. Bronchoalveolar lavage and protected distal brushings were carried out. Both Aeromonas hydrophila and Staphylococcus aureus were found in the cultured brushings. Treatment with ceftriaxone, vancomycin and amikacin was introduced. This nosocomial pneumonia was very haemorrhagic, resulting in several bloody casts responsible for several episodes of atelectasis. The patient was definitely extubated on the 18th day, and left the ICU 23 days later without any sequela. His HIV status was negative. Four other infections with the same strain of Aeromonas hydrophila occurred at the same time as this patient's. The common source for this germ was found to be soft water. Several measures have since been undertaken: removal of a centralized water softener, filtration and higher chlorine content in the water circuit, and updating of intensive care protocols for disinfection of equipment.

Acebutolol↗
PubMed1986

[Retrospective diagnosis of a coma in an infant].

A four month old baby presented one morning a quiet, hypotonic, areflexive coma without any signs of localization, which vanished without any sequelae. Hepatic cytolysis and an isolated proteinuria with a maximum at about three days after the initial neurological problems completed the picture. A new interview with the parents looking for a toxic cause revealed without any doubt poisoning by tetrachloro-ethylene. Following this particular case, the main signs of poisoning by halogenated aliphatic hydrocarbons are recalled. One should always have in mind the possibility of poisoning at all ages, even with young babies.

Acidosis↗
PubMed1989

[Hypokalemic quadriplegia and coma in renal tubular acidosis].

A case is reported of an acute episode of severe hypokalaemia (K+ = 1.1 mmol.l-1) associated with hyperchloraemic acidosis and simultaneous high urine pH (pH = 7) in a 24 year old woman with type I distal tubular acidosis and nephrocalcinosis. The flaccid paralysis involved the trunk, neck, facial and pharyngeal muscles. She was in areflexic quadriplegia, coma and respiratory failure requiring endotracheal intubation and positive pressure ventilation. There were no cardiac disturbances, presumably because of the chronic potassium depletion, the patient's youth and healthy myocardium. Despite the usually recommended maximal potassium infusion rate (0.25 mmol.kg-1.h-1), there was a transient worsening of her neuromuscular status. Only 12 h later, the first movements were noticed. In order to prevent such a deterioration, a more rapid potassium infusion could have been used. However, in our case, the occurrence of hypokalaemic extrasystoles was reduced and the patient was still intubated and ventilated. It was therefore decided not to run the risk of myocardial inexcitability carried out with supramaximal infusion rates and to keep the usual protocol. Besides, several pitfalls have to be avoided during the treatment of the numerous metabolic disorders coexisting with severe hypokalaemia, such as metabolic acidosis and hyperglycaemia.

Acidosis, Renal Tubular↗
PubMed1997

[Use of Glasgow coma scale by anesthesia and intensive care internists in brain injured patients].

OBJECTIVE: To evaluate the quality and reliability of the Glasgow coma scale (GCS) score when determined, in head trauma patients, by trainees in anaesthesiology. STUDY DESIGN: Prospective survey. USERS: One hundred trainees in their first to fourth year of training in anaesthesiology. METHODOLOGY: A questionnaire completed by the trainees concerning: demographic data; place, time and qualification of the physician determining the first GCS score; time and qualification of the physician determining the subsequent GCS score; assessment of the GCS score in case of asymmetrical motor response, tracheal intubation, bilateral eyelid oedema, or circulatory or ventilatory failure. RESULTS: Sixty questionnaires were available for analysis. Lack of compliance with the rules for the GCS score evaluation resulted in many errors by most of the trainees. Only a few of them determined an accurate GCS score in cases of asymmetric motor response or impossibility to determine verbal or ocular response. Finally, GCS scores were determined later only very rarely. CONCLUSION: In order to provide optimal care and allow an accurate assessment of therapeutic efficiency, special attention should be given to the teaching of the GCS scoring method in head trauma patients.

Anesthesiology↗
PubMed1997

[Severe form of familial migraine with coma].

The authors report the case of a 43-year-old man experiencing a migraine attack with coma requiring a treatment in an intensive care unit for 9 days. The probable triggering cause as a cerebral arteriography.

Adult↗
PubMed2002

Wide clinical variability in a family with a CACNA1A T666m mutation: hemiplegic migraine, coma, and progressive ataxia.

We report a Japanese family carrying a T666M missense mutation of CACNA1A. Affected members demonstrated a strikingly wide clinical spectrum including migraine, hemiplegia, coma, and progressive cerebellar ataxia. Despite such variability of the clinical features, they demonstrated similar magnetic resonance imaging findings demonstrating cerebellar atrophy predominantly of the cerebellar vermis. These magnetic resonance images appeared not to correlate with clinical severity. Our findings should indicate that a T666M mutation of CACNA1A may be associated with more variable clinical features and that paroxysmal hemiplegic migraine attacks and progressive cerebellar atrophy should have distinct mechanisms of pathogenesis.

Adult↗
PubMed2000

Coma as an acute presentation of adrenoleukodystrophy.

X-linked adrenoleukodystrophy is a metabolic disorder with broad clinical variations. A 4-year-old male admitted to the hospital with fever, hypotension, and coma as the presenting signs of adrenoleukodystrophy is reported. The initial presentation followed by rapidly developing disseminated intravascular coagulopathy and multiorgan failure suggested an initial diagnosis of septic shock. However, bronze skin pigmentation and a cranial computed tomography scan demonstrating posterior demyelination consistent with adrenoleukodystrophy led to the final diagnosis. The diagnosis was confirmed by the findings of elevated very-long-chain fatty acid levels and an elevated C24/C16 ratio in plasma and fibroblast cultures. Atypical presentations of the disease require a high index of suspicion to initiate treatment before the appearance of irreversible sequelae.

Acute Disease↗
PubMed1997

Carotid arterial trauma: assessment with the Glasgow Coma Scale (GCS) as a guide to surgical management.

Management of carotid arterial injuries associated with focal neurological deficit or altered state of consciousness (SCON) remains unresolved. Experience with these injuries in one particular hospital was reviewed and the Glasgow Coma Scale (GCS) utilized to assist with clinical stratification of these patients. A literature review was also conducted to better define indications for repair or ligation of carotid injuries. From 1978 to 1990, 34 patients with carotid arterial injuries were reviewed with reference to the GCS, focal deficit, hypotension, anatomic site and mechanism of injury. The literature from 1952 to 1993 was surveyed for carotid artery injuries (1316 patients). Outcome of treatment with or without repair was compared with pre-operative neurologic status. Thirty-four patients with injuries of the common (24) or internal (10) carotid arteries were managed with repair (68%), ligation (24%) or observation (9%). The SCON was normal in 18 patients; 16 patients (88%) underwent repair and all remained normal. All patients with GCS 9-14 regained a normal SCON after surgical repair, while 10 patients with GCS < 8 had repair (5), ligation (3), and non-operative management (2); five returned to normal, four died and one remained comatose. However, outcomes correlated poorly with management. Of 1316 patients cited in the surgical literature, patients with no deficit and patients with pre-operative deficits did significantly better after repair as compared with ligation (P<0.001). In comatose patients, management did not affect outcome. It is concluded that carotid arterial injuries should be repaired in patients with normal neurologic evaluation, focal pre-operative neurologic deficits and in patients with GCS > 9. Comatose patients with GCS < 8 do poorly regardless of management. The GCS provides an objective for stratification of patients with altered SCON who benefit from repair of carotid arterial injuries.

Adult↗
PubMed1993

[Early somatosensory (SEP) and auditory (AEP) evoked potentials in anoxic coma: prognostic value].

Early somatosensory (SEP) and auditory (BAEP) evoked potentials, when recorded within the first seven days of the course of anoxic coma, appear to be reliable to evaluate anoxic ischemic cortical or under-cortical lesions. Prognosis depends especially on cortical SEP (N20-P25): the lack of SEP is a good outcome predictor of death (abnormal BAEP) or of vegetative status (normal BAEP); the presence of normal and bilateral cortical SEP (with normal BAEP) allows to predict awakening, without prejudging of neurologic sequelae, even if they are severe.

Acoustic Stimulation↗
PubMed1989

[Contribution of the EEG and evoked potentials in the prognosis of post-anoxic comas in children].

Six children with post-anoxic coma were studied and there was evidence of preserved brainstem function together with the presence of electrocerebral activity on EEG. There is no definite prognosis with slow EEG; patients can either die, survive, but with major neurological damage, or recover completely. In that case, evoked potentials have a good prognostic value. Normal BAEP indicate that patients will survive. However, absence of the cortical component of SEP indicates major cerebral damage. Evolution towards a vegetative state can therefore be predicted.

Adolescent↗
PubMed2004

Somatosensory evoked potentials in coma prognosis.

SEPs provide useful prognostic information regarding outcome after coma. Use of the summary data presented here should allow clinicians caring for these patients to provide families with a greater degree of certainty regarding outcome than previously has been available.

Brain Injuries↗