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Martin Holtkamp

Publications and source records attributed to Martin Holtkamp.

12 recordsLinked to original sources
PubMed2006

Temperature regulation is compromised in experimental limbic status epilepticus.

Temperature dysregulation is well known in generalized convulsive status epilepticus but so far has not been reported in non-convulsive forms. In order to detect possible subtle alterations, we have analyzed the capability to compensate for external cooling in an animal model of limbic status epilepticus. Rats with electrically induced self-sustaining status epilepticus (SSSE) (n=6) as well as rats without electrical stimulation (n=6) were cooled for 3 h and then rewarmed for another hour. The time course of changes in epidural temperature in animals of both groups that underwent cooling and in control rats that were not cooled and not stimulated (n=6) was compared. In animals with limbic SSSE, temperature fell continuously and was significantly lower at all time points under cooling as compared with each of the two other groups. In animals that were not stimulated, temperature under cooling fell by 1 to 2 degrees C only and was not significantly different at any time point as compared with controls. The effect of cooling was reversible in both groups. The current data indicate that temperature homeostasis in limbic status epilepticus is markedly disturbed. This finding may suggest ictal involvement of primary thermoregulatory neurons in the anterior hypothalamus probably by spread of epileptic activity from temporo-mesial structures.

Animals↗
PubMed2006

Diagnosis of psychogenic nonepileptic status epilepticus in the emergency setting.

Episodes of psychogenic nonepileptic status epilepticus (PNESE) characterized by pronounced generalized motor features were compared with those of refractory generalized convulsive status epilepticus. Patients with PNESE were younger, had port systems implanted more frequently, received higher doses of benzodiazepines until seizure termination or respiratory failure, and had lower serum creatine kinase levels.

Aged↗
PubMed2005

Functional, cognitive and emotional long-term outcome of patients with ischemic stroke requiring mechanical ventilation.

Prognosis of patients with ischemic stroke requiring mechanical ventilation (MV) has been reported to be poor. However, longterm survival and functional outcome have scarcely been studied and nothing is known about the prevalence of cognitive impairment or depression in survivors and their quality of life (QoL). We identified all patients treated for acute ischemic stroke on a Neurological Intensive Care Unit during 3.5 years who required MV for more than 24 hours. Early mortality rate at 2 months and survival rates at 1 and 2 years were determined. Survivors were examined for functional outcome (modified Rankin Scale (mRS), Barthel Index), cognitive impairment (Mini Mental State Examination (MMSE)), depression (Beck Depression Inventory, BDI) and QoL (Short Form-36). Clinical characteristics on admission were analyzed for prognostic significance. Of 101 consecutive patients, 44% died within 60 days. Survival rates at 1 and 2 years were 40% and 33%, respectively. Age > 60 years (p = 0.002) and Glasgow Coma Scale score < 10 on admission (p = 0.002) were independent predictors of early and late mortality. History of myocardial infarction (p = 0.007) independently predicted late mortality at 2 years. Of 33 surviving patients, nine (27%) had a good functional outcome (mRS 0-2). Of 27 survivors who could be interviewed, 17 (63%) had no cognitive impairment (MMSE > 24) and 20 (74%) did not suffer from relevant depression (BDI < 19). In conclusion, longer-term survival of patients with ischemic stroke requiring MV was 33% and every fourth survivor resumed an independent life without dementia or depression. Older patients comatose on admission and with concomitant cardiovascular disease had the lowest probability of a favorable outcome.

Aged↗
PubMed2005

A "malignant" variant of status epilepticus.

BACKGROUND: Status epilepticus (SE) frequently does not respond to common first-line anticonvulsants. In a substantial portion of patients, administration of anticonvulsant anesthetics is inevitable. Even this aggressive approach fails to terminate SE in an undefined number of cases. We have coined the term malignant SE for this most severe variant of SE. OBJECTIVE: To assess frequency, risk factors, and in-hospital outcome of malignant SE. DESIGN: Retrospective cohort study. SETTING: Neurologic intensive care unit of a large university hospital. Patients Sample of 35 episodes of SE not responding to first-line anticonvulsants in 34 patients. MAIN OUTCOME MEASURES: Predictive and prognostic features of episodes of malignant SE with persistent epileptic activity after high-dose anesthetics compared with features of the remainder of cases with refractory SE and persistent epileptic activity after failure of first-line anticonvulsants. RESULTS: Status epilepticus that could not be controlled by first-line anticonvulsants resulted in malignant SE in 20% of cases. Patients with malignant SE were significantly younger than patients with refractory SE (P = .03). Encephalitis was identified as an independent risk factor for malignant SE (P = .008). Outcome in malignant SE was poor, with significantly longer duration of seizure activity (P<.001), longer stay in the neurologic intensive care unit (P<.001) and in the hospital (P = .007), and more patients with functional dependency at discharge from the hospital (P = .04). CONCLUSIONS: Malignant SE is not rare after failure of first-line anticonvulsants. The patient at risk is typically young and suffers from encephalitis. Such patients should be treated aggressively early in the course of SE to prevent malignant SE.

Adolescent↗
PubMed2005

Limbic self-sustaining status epilepticus in rats is not associated with hyperthermia.

PURPOSE: To evaluate the impact of limbic status epilepticus on temperature. METHODS: The perforant path in freely moving rats was stimulated electrically for 120 min to induce self-sustaining status epilepticus (SSSE). For 150 min after the end of stimulation, epidural temperature and electrographic and clinical seizure activity were assessed in animals with limbic and motor SSSE, as well as in animals without development of SE. RESULTS: Temperature in all animals with SSSE was elevated by 1.5+/-0.8 degrees C after the end of stimulation compared with baseline values (p<0.01). In animals with pure limbic SE, temperature decreased continuously to baseline values over the 150-min period of observation. In contrast, in animals with motor SSSE, temperature remained elevated during continuing epileptic activity and was still significantly higher 150 min after the end of stimulation compared with baseline (p<0.01). In animals that did not develop SSSE, temperature was not changed after the end of electrical stimulation and in the 150 min thereafter compared with baseline values. CONCLUSIONS: The results indicate that hyperthermia as seen in SE is the consequence of motor convulsions and not of epileptic activity itself, as seen in limbic SSSE.

Animals↗
PubMed2004

Recurrent seizures do not cause hippocampal damage.

Neuronal consequences of recurrent single epileptic seizures have been discussed controversially for some time. Various cross-sectional magnetic resonance imaging (MRI) studies have shown a positive correlation between the severity of epilepsy and the extent of hippocampal damage. However, the open question whether recurrent epileptic seizures induce hippocampal structural pathology can be assessed only in longitudinal studies. The few recent follow-up studies have revealed conflicting results. In the current MRI study we have employed volumetry and T2 relaxometry to quantify hippocampal structural changes of patients with chronic partial epilepsies over a period of 3 years. Our main findings demonstrate that these patients who experience continuing epileptic seizures do no show any development of new pathology or any relevant deterioration of pre-existing hippocampal structural lesions. This argues against the assumption that recurrent epileptic seizures cause or increase structural hippocampal damage.

Adult↗
PubMed2003

Furosemide terminates limbic status epilepticus in freely moving rats.

PURPOSE: To evaluate the anticonvulsant properties of furosemide and to determine sedative side effects compared with pentobarbital and diuretic side effects compared with saline-treated controls in an experimental model of limbic status epilepticus. METHODS: Self-sustaining status epilepticus was induced in rats by continuous electrical stimulation of the perforant path. Five minutes after the end of the stimulation, animals were given 100 mg/kg furosemide, 30 mg/kg pentobarbital, or an equal amount of saline, intraperitoneally. After administration of the substance, animals were monitored clinically and electrographically for 3 h regarding status epilepticus, level of sedation, and diuresis. RESULTS: In seven of 10 animals, furosemide terminated status epilepticus after 68 +/- 26 min, whereas pentobarbital was successful in all animals after 5 +/- 0.8 min. In contrast to pentobarbital, sedation did not occur with furosemide. Weight loss after furosemide was 10.2 +/- 1.7% compared with 6.5 +/- 1.1% in animals given saline (p < 0.001). CONCLUSIONS: The results suggest that furosemide may serve as an alternative or additional agent for refractory complex partial status epilepticus in patients in whom common anesthetics are not justifiable.

Animals↗
PubMed2002

Intrinsic optical imaging reveals regionally different manifestation of spreading depression in hippocampal and entorhinal structures in vitro.

The spatiotemporal features of spreading depression (SD) were analyzed in vitro by using combined hippocampal-entorhinal cortex slices. SDs were induced by microinjection of 1 M KCl in the stratum radiatum of the CA1 region of the hippocampus. Measurements of extracellular field potentials, extracellular space (ECS) volume changes and intrinsic optical signal changes were combined to study SD features in different regions of the slice. Each SD was associated with a pronounced shrinkage of the extracellular space (ECS) volume and a decrease in light transmittance. The beginning of the optical signal change occurred simultaneously with the electrographic onset as measured with extracellular microelectrodes but outlasted the dc shift for tens of seconds. The amplitude of the intrinsic optical signal change displayed marked regional variations with greatest changes of 12% in cortical regions. The signal amplitudes were considerably lower in hippocampal regions. The analysis of spread patterns revealed two types of waves: fully propagated waves spreading from CA1 all the way to the temporal neocortex and abortive waves that ceased earlier. The spread velocities displayed pronounced regional differences with highest velocities of 5.4 +/- 0.3 mm/min in the area CA3 of the hippocampal formation and lowest velocities of 2.7 +/- 0.1 mm/min in cortical regions.

Animals↗