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Biomedical subjects

E Hund

Publications and source records attributed to E Hund.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Transtracheal monitoring of the recurrent laryngeal nerve. Prototype of a new tube].

A new sensing device for the continuous intraoperative monitoring of the recurrent laryngeal nerve is presented. It is based on a double ballooned endotracheal tube including stimulating and tracing electrodes. The system is characterised by three advantages: 1) it is atraumatic, 2) it is operating completely outside the operating field (extraterritorially), 3) nerve function is being monitored continuously from the time of intubation to the time of extubation. The presented system has been evaluated in piglets. First results in humans will be available shortly.

Animals↗
PubMed1997

[Infection: impaired consciousness as the initial symptom. Clinical and pathophysiologic aspects of septic encephalopathy].

Septic encephalopathy (SE) is present in up to 70% of all patients with sepsis. In some cases, SE may proceed other parameters of sepsis. Loss of consciousness to a various extent is the leading symptom. CSF findings and CCT are usually unremarkable. EEG is a sensitive parameter to monitor SE. EEG-changes deteriorate in correspondence to the degree of SE. If sepsis can be treated successfully, clinical and electrophysiological signs are completely reversible. SE has a complex etiology. Bacterial endotoxins and other microbial products trigger the release of a multitude of mediators of sepsis. Due to liver dysfunction in sepsis, the brain neurotransmitter profile may be deranged. Other etiological factors include bacteriemia, liver or renal dysfunction, fluid and electrolyte imbalance, hypoglycemia and drug effects. Due to the prognostic significance of early adequate treatment, recognition of SE as a possible initial sign may be crucial for patients with sepsis.

Aged↗
PubMed1997

Progressive cerebellar ataxia, proximal neurogenic weakness and ocular motor disturbances: hexosaminidase A deficiency with late clinical onset in four siblings.

Tay-Sachs disease is a genetically determined neurodegenerative disorder, resulting from mutations of the hexosaminidase (Hex) A gene coding for the alpha-subunit of beta-D-N-acetyl-hexosaminidase. Clinically, there is severe encephalomyelopathy leading to death within the first few years of life. Hex A activity is usually absent in tissue and body fluids of these patients. Juvenile and adult Hex A deficiencies are less severe but rare variants with some residual Hex A activity. All these variants are most prevalent among Ashkenazi Jews. We describe a non-Jewish family in which four adult brothers and sisters had markedly reduced Hex A activities and onset of symptoms in the second decade of life. The phenotypical expression was remarkably homogeneous, consisting in a combination of slowly progressive motor neuron disease, ataxia and ocular motor disturbances. None of the patients were demented at this stage of their illness. Magnetic resonance studies showed severe cerebellar atrophy, but were otherwise normal. Hex A deficiency was established by biochemical measurements in the serum and skin fibroblasts using the fluorogenic substrates 4-MUG and 4-MUGS as well as by gel electrophoresis. Molecular genetic studies revealed that the patients are compound heterozygotes for the 'adult' mutation Gly269 --> Ser and the 'infantile' 4-base insertion in exon 11 of the Hex A gene.

Adult↗
PubMed1997

Critical illness polyneuropathy: a new iatrogenically induced syndrome after cardiac surgery?

OBJECTIVE: Critical illness polyneuropathy (CIP) is a newly described severe complication after open heart surgery leading to tetraplegia for weeks to months. The purpose of the study was to gather further information on critical illness polyneuropathy developing in patients after cardiac surgery and to evaluate the hypothetical risk factors possibly related to the onset of this neurological disorder. METHODS: From July 1994 to October 1995, 7 out of 1511 patients undergoing open heart surgery developed critical illness polyneuropathy, which was diagnosed on the basis of electromyographic and nerve conduction features. The only common clinical finding was an intensive care unit (ICU) stay beyond seven days, therefore a similar group of 37 patients staying longer than seven days in the intensive care unit during the same period of time was evaluated and retrospectively compared to the 7 patients developing critical illness polyneuropathy. Univariate analysis of several traits was performed to evaluate possible risk factors. RESULTS: 4 Out of 7 patients in the CIP group died, all due to multiple organ failure, in contrast to 3/37 patients in the control group, again due to multiple organ failure. Patients developing CIP were staying significantly longer in the ICU (62+/-3 versus 14+/-8 days, P < 0.01) and had a significantly longer time on ventilator support (50+/-28 versus 7+/-13 days, P < 0.01) The incidence of sepsis was significantly higher in the CIP group than in the control group (85.7 versus 10.8%, P < 0.01). Compared to the control group the proportion of patients receiving corticosteroids (100 versus 10.8%, P < 0.01) and increased dosages of epinephrine and norepinephrine was higher in the CIP group (85.7 versus 35.1%, P < 0.05). Furthermore, the proportion of patients requiring chronic venovenous hemodiafiltration was significantly elevated in the CIP group (85.7 versus 5.4%, P < 0.01). CONCLUSIONS: CIP, despite it's benign nature due to it's spontaneous remission in patients who survive, is a disturbing complication following cardiac surgery which is associated with high mortality, a prolonged stay in the ICU, as well as an extended time on ventilator support. Interventions like chronic hemodiafiltration, the application of corticosteroids and the administration of high doses of catecholamines are more frequent in patients with CIP. Whether this indicates a causal relationship remains to be elucidated.

Adrenergic alpha-Agonists↗
PubMed1997

Predominant involvement of motor fibres in patients with critical illness polyneuropathy.

Critical illness polyneuropathy (CIP) is a recognized cause of muscle weakness and failure of weaning from a ventilator. In order to characterize the features of CIP, we have examined 28 consecutive surgical patients with severe sepsis using bedside electrophysiology. Of the 28 patients (median APACHE II score 31), 20 developed moderate to severe CIP, as shown by the presence of moderate to severe denervation activity on resting EMG. The median nerve compound muscle action potential (CMAP) amplitudes were reduced to 3.24 (SEM 0.48) mV, while sensory nerve action potential (SNAP) amplitudes obtained from the same nerve were normal (13.1 (1.9) microV). In approximately 50% of these patients, the reduction in CMAP exceeded 50% of the lower limit of normal. Similar results were obtained from stimulation of the ulnar nerve. We conclude that CIP is a major complication in patients with severe sepsis and prolonged artificial ventilation. It predominantly involves motor fibres and thus markedly interferes with weaning from the ventilator.

Adolescent↗
PubMed1997

Serum neuron-specific enolase as early predictor of outcome after cardiac arrest.

OBJECTIVE: To examine the prognostic value of serum neuron-specific enolase for early prediction of outcome in patients at risk for anoxic encephalopathy after cardiac arrest. DESIGN: Prospective study. SETTING: Coronary intensive care unit of the University of Heidelberg. PATIENTS: Forty-three patients (66.8 +/- 12.7 [SD] yrs, range 33 to 85) who had had either primary or secondary cardiac arrest, followed by cardiopulmonary resuscitation (CPR). INTERVENTIONS: Serial blood samples and clinical examinations. MEASUREMENTS AND MAIN RESULTS: Serum neuron-specific enolase concentrations were determined after CPR on 7 consecutive days. Twenty-five patients remained comatose and subsequently died; 18 patients survived the first 3 months and had no relevant functional deficit at 3-month follow-up. Neuron-specific enolase concentrations were correlated with neurologic outcome. Concentrations of >33 ng/mL predicted persistent coma with a high specificity (100%) and a positive predictive value of 100%. Overall sensitivity was 80%, with a negative predictive value of 78%. Serum concentrations of neuron-specific enolase exceeded this cutoff value no more than 3 days after cardiac arrest in 95% of patients in whom these concentrations had exceeded 33 ng/mL. CONCLUSIONS: In patients who have been resuscitated after cardiac arrest, serum neuron-specific enolase concentrations of >33 ng/mL predict persistent coma with a high specificity. Values below this cutoff level do not necessarily indicate complete recovery, because this method has a sensitivity of 80%.

Adult↗
PubMed1997

Proximal myotonic myopathy with MRI white matter abnormalities of the brain.

Proximal myotonic myopathy (PROMM) is an autosomal dominantly inherited multisystemic disorder characterized by myotonia, proximal muscle weakness, and cataracts. This disorder is not linked to the gene locus of myotonic dystrophy (DM). We describe three new families with PROMM. In all patients, CTG repeats of the DM gene in DNA from blood leukocytes were normal. MRI of the brain revealed a consistent pattern of marked white matter hyperintensity on T2-weighted images in four patients; two additional patients had similar but mild to moderate MRI abnormalities. The morphology of these abnormalities is unknown. Clinical symptoms of brain disease were not consistent and included mental changes with hypersomnia, parkinsonian features, stroke-like episodes, and seizures. The causative relationship of these clinical features with the MRI white matter abnormalities remains to be established. Our observations suggest that PROMM may involve the brain.

Adult↗
PubMed1997

Neurocritical care for acute ischemic stroke.

Treatment strategies for acute ischemic stroke include general and specific measures. The rationale for these strategies is discussed, and the current practice in the acute phase of ischemic stroke is presented. Special attention is given to the patient requiring intensive care.

Adult↗
PubMed1996

"Sunbath polyneuritis": subacute axonal neuropathy in perazine-treated patients after intense sun exposure.

This article aims at drawing attention to the peculiar association of intense exposure to sunlight and subacute development of sensory neuropathy which was seen in 7 psychiatric patients treated with the phenothiazine derivative, perazine. Three patients additionally developed bilateral VII nerve palsy. Symptoms followed a monophasic course with almost complete remission. Routine neurophysiology suggested axonal neuropathy confirmed by sural nerve biopsy in 1 patient. A toxic origin of neuropathy is supposed, possibly induced by phenothiazine photoproducts, which may cause cell damage via lipid peroxidation.

Adult↗
PubMed1996

A transgenic rat model of Charcot-Marie-Tooth disease.

Charcot-Marie-Tooth disease (CMT) is the most common inherited neuropathy in humans and has been associated with a partial duplication of chromosome 17 (CMT type 1A). We have generated a transgenic rat model of this disease and provide experimental evidence that CMT1A is caused by increased expression of the gene for peripheral myelin protein-22 (PMP22, gas-3). PMP22-transgenic rats develop gait abnormalities caused by a peripheral hypomyelination, Schwann cell hypertrophy (onion bulb formation), and muscle weakness. Reduced nerve conduction velocities closely resemble recordings in human patients with CMT1A. When bred to homozygosity, transgenic animals completely fail to elaborate myelin. We anticipate that the CMT rat model will facilitate the identification of a cellular disease mechanism and serve in the evaluation of potential treatment strategies.

Animals↗
PubMed1995

Inclusion body myositis presenting with isolated erector spinae paresis.

We report a 70-year-old patient who presented with a 4-year history of weakness of paravertebral muscles. Electrodiagnostic studies revealed a mixed neurogenic-myopathic pattern. Light microscopic examination revealed atrophic fibers with rimmed vacuoles; electron microscopy demonstrated cytoplasmic and intranuclear filaments measuring about 16 nm in width, consistent with the diagnosis of inclusion body myositis. Therapy with corticosteroids provided only a mild and transient benefit. Ten months after the initial evaluation, clinical and electrodiagnostic examination demonstrated mild progression of the disease.

Aged↗
PubMed1995

Neurocritical care for acute ischemic stroke.

Therapy for acute ischemic stroke includes general and specific measures. General management such as respiratory and cardiac care, fluid and electrolyte management, blood pressure control, and treatment of increased ICP is the basis of all stroke treatment. Specific treatment is directed to recanalization of the occluded vessel, control of life-threatening brain edema, and protection of neuronal tissue against the toxic effects of ischemia. Although controlled studies are still lacking, application of the proposed general interventions provides a high-quality standard in patients with acute stroke. Among specific therapies, medical thrombolysis has demonstrated instances of significant and sustained neurologic improvement. Several multicenter trials are underway to confirm these preliminary results. In addition to thrombolysis, cell-protecting drugs hold promise for the future. Presumably, a combination of thrombolytic and cell-protecting agents will be the treatment of choice in early stroke in the future.

Acute Disease↗
PubMed1995

[Craniectomy in space-occupying middle cerebral artery infarcts].

Space occupying supratentorial ischemic stroke has a high mortality. The benefit of decompressive surgery in these patients is still matter of debate. In a prospective study we performed craniectomy in 37 patients with acute middle cerebral artery infarction and progressive deterioration under conservative antiedematous therapy. Twenty-one patients treated conservatively during the same period served as control group. All survivors were reexamined between one to two years after surgical decompression. In addition, neuropsychological tests were performed, including an Aachener Aphasie Test (AAT) in those patients with infarction of speech-dominant hemisphere. Clinical evaluation was graded using the Barthel index (BI). Mortality rate in the operated group was 37%. Twenty-three patients survived acute stroke and were reexamined. Despite complete hemispheric infarction, no patient suffered from complete hemiplegia or was permanently wheel chair bound. In speech dominant hemispheric infarction (n = 8) only mild to moderate aphasia could be detected. Mean BI was 64. Mortality rate in the conservatively treated group was 76%. The clinical outcome following craniectomy for the treatment of severe ischemic hemispheric infarction is unexpectedly good. Therefore, decompressive surgery should be considered in cases of space-occupying hemispheric infarctions and conservatively uncontrollable intracranial pressure.

Adolescent↗
PubMed1993

[Experiences with high dosage immunoglobulin G in neuromuscular diseases].

High-dose intravenous immunoglobulin G (IVIG) was used as alternative treatment in 39 patients with crisis in myasthenia gravis (MG), acute polyneuritis (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Of 10 patients with MG, 3 recovered completely, 5 patients improved except for long-standing ocular signs, 1 patient was weaned from artificial ventilation, and one patient did not improve after IVIG, but did so after plasma exchange. 25 GBS patients were treated with IVIG, progression of weakness was stopped in 24; 12 showed complete or near complete recovery and 6 improved markedly. Of 4 patients with CIDP, 2 responded definitely. The majority of patients with MG, GBS, CIDP, respond to IVIG treatment. The effect seems to be equivalent to plasma exchange. In GBS, IVIG may be superior. Side effects of IVIG are negligible, and there is no risk of transmission of AIDS-, hepatitis-, or other viruses.

Adult↗