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C Helmchen

Publications and source records attributed to C Helmchen.

53 records · Page 3Linked to original sources
PubMed1996

Reversible hepatotoxicity of paroxetine in a patient with major depression.

Selective serotonin reuptake inhibitors (SSRIs) are becoming widely used because of their favorable side-effect profile and their safety in overdose. We report about a patient with recurring major depression (DSM-IIIR) who was treated with paroxetine and developed a severe hepatotoxic reaction, which was reversed after withdrawal of the drug. Individual, patient-related causes for this side-effect were not found. To our knowledge, this is the first published case of a probably paroxetine-induced severe hepatotoxicity. Hepatotoxicity should be taken into account as a rare complication that may occur not only with tricyclic antidepressants (TCAs) but also with SSRIs.

Antidepressive Agents, Second-Generation↗
PubMed1996

Contralesionally beating torsional nystagmus in a unilateral rostral midbrain lesion.

The rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and the interstitial nucleus of Cajal (iC) are involved in the generation of vertical and torsional saccades and gaze holding. Midbrain lesions involving either riMLF or iC produce a tonic torsional ocular deviation to the contralesional side. Lesions of the iC are associated with an ipsilesional torsional nystagmus (TN). For the first time, we describe a patient with a unilateral midbrain lesion showing a contralesionally beating torsional nystagmus. This nystagmus was probably caused by a lesion involving the riMLF.

Brain Diseases↗
PubMed1995

Inhibition of spinal nociceptive neurons by microinjections of somatostatin into the nucleus raphe magnus and the midbrain periaqueductal gray of the anesthetized cat.

The effects of somatostatin (SOM) after intravenous application and intracerebral microinjection into the medullary nucleus raphe magnus (NRM) or into the periaqueductal gray (PAG) on the spinal nociceptive transmission was quantitatively studied in the anesthetized cat. Noxious heat-evoked responses of multireceptive lumbar spinal dorsal horn neurons were reversibly depressed to 56.6 +/- 9.7% of the control after systemically applied SOM (7 micrograms/kg i.v.; 7 micrograms/kg per h infusion rate). At 11 of 14 brainstem microinjection sites in the NRM and PAG, SOM (2.5 micrograms/microliter) attenuated the heat-evoked responses to 58.9 +/- 6.2% (n = 5) (NRM) and 64.4 +/- 6.3% (n = 6) (PAG) of the control. After microinjection, maximal inhibition was reached within 8-14 min (NRM) or 23-29 min (PAG), respectively. Inhibition was reversible within 60 min after the injection. Thus, SOM has an antinociceptive potency by activating descending inhibition of nociceptive dorsal horn neurons from the NRM and PAG.

Animals↗
PubMed1995

Saccade-related Purkinje cell activity in the oculomotor vermis during spontaneous eye movements in light and darkness.

Saccade-related Purkinje cells (PCs) were recorded in the oculomotor vermis (lobules VI, VII) during spontaneous eye movements and fast phases of optokinetic and vestibular nystagmus in the light and darkness, from two macaque monkeys. All neurons (n = 46) were spontaneously active and exhibited a saccade-related change of activity with all saccades and fast phases of nystagmus. Four types of neurons were found: most neurons (n = 31) exhibited a saccade-related burst of activity only (VBN); other units (n = 7) showed a burst of activity with a subsequent pause (VBPN); some of the units (n = 5) paused in relation to the saccadic eye movement (pause units, VPN); a few PCs (n = 3) showed a burst of activity in one direction and a pause of activity in the opposite direction. For all neurons, burst activity varied considerably for similar saccades. There were no activity differences between spontaneous saccades and vestibular or optokinetically elicited fast phases of nystagmus. The activity before, during, and after horizontal saccades was quantitatively analyzed. For 24 burst PCs (VBN, VBPN), the burst started before saccade onset in one horizontal direction (preferred direction), on average by 15.3 ms (range 27-5 ms). For all these neurons, burst activity started later in the opposite (non-preferred) direction, on average 4.9 ms (range 20 to -12 ms, P < 0.01) before saccade onset. The preferred direction could be either with ipsilateral (42% of neurons) or contralateral (58%) saccades. Nine burst PCs had similar latencies and burst patterns in both horizontal directions. The onset of burst activity of a minority of PCs (n = 5) lagged saccade onset in all directions. The pause for VBPN neurons started after the end of the saccade and reached a minimum of activity some 40-50 ms after saccade completion. For all saccades and quick phases of nystagmus, burst duration increased with saccade duration. Peak burst activity was not correlated with saccade amplitude or peak eye velocity. PCs continued to show saccade-related burst activity in the dark. However, in 59% of the PCs (VBN, VBPN), peak burst activity was significantly reduced in the dark (on average 28%, range 15-36%) when saccades with the same amplitude (but longer duration in the dark) were compared. For VBP neurons, the pause component after the saccade disappeared in the dark.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

[Therapy of cerebral aneurysms and arteriovenous vascular malformations in hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease)].

Little is known about the course of cerebral aneurysms in hereditary hemorrhagic teleangiectasia (Rendu-Osler-Weber's disease). Thus, therapeutic decisions are often difficult. For the first time, we report the successful embolization of an arteriovenous fistula and multiple aneurysms of the posterior inferior cerebellar artery (PICA) of a patient with Rendu-Osler-Weber's disease after subarachnoid hemorrhage. Two years later she suffered another severe intracranial hemorrhage. Angiography revealed an aneurysm in the same artery (PICA), which spontaneously disappeared within 2 months. Spontaneous regression of aneurysms in Rendu-Osler-Weber's disease has not been reported before.

Cerebellum↗
PubMed1994

Saccade-related activity in the fastigial oculomotor region of the macaque monkey during spontaneous eye movements in light and darkness.

Saccade-related burst neurons were recorded in the caudal part of the fastigial nucleus (fastigial oculomotor region) during spontaneous eye movements and fast phases of optokinetic and vestibular nystagmus in light and darkness from three macaque monkeys. All neurons (n = 47) were spontaneously active and exhibited a burst of activity with each saccade and fast phase of nystagmus. Most neurons (n = 31) only exhibited a burst of activity, whereas those remaining also exhibited a pause in firing rate before or after the burst. Burst parameters varied considerably for similar saccades. For horizontal saccades all neurons, except for three, had a preferred direction with an earlier onset of burst activity to the contralateral side. For contralateral saccades the burst started on average 17.5 ms before saccade onset, whereas the average lead-time for ipsilateral saccades was only 6.5 ms. Three neurons were classified as isotropic with similar latencies and peak burst activity in all directions. None of the neurons had a preferred direction with an earlier onset of burst activity to the ipsilateral side. Burst duration increased with saccade amplitude, whereas peak burst activity was not correlated with amplitude. There was no relationship between peak burst activity and peak eye velocity. In the dark, neurons generally continued to burst with each saccade and fast phase of nystagmus. Burst for saccades in the dark was compared with burst for saccades of similar amplitude and direction in the light. Saccades in the dark had a longer duration and peak burst activity was reduced on average to 62% (range 36-105%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Saccadic lateropulsion in Wallenberg's syndrome may be caused by a functional lesion of the fastigial nucleus.

One of the clinical oculomotor hallmarks of lateral medullary infarction (Wallenberg's syndrome) is the so-called saccadic lateropulsion. In man and in animals, cerebellar lesions lead to dysmetric saccades and underline the importance of cerebellar control on saccadic accuracy. In order to study the lesion site responsible for saccadic lateropulsion we prospectively examined 12 patients with Wallenberg's syndrome who did not show a cerebellar lesion on CT or MRI. All patients consistently showed hypermetric saccades to the ipsilateral side and hypometric contralateral saccades comparable with the effects of cerebellar lesions in monkeys on saccadic accuracy. Based on the most recent experiments involving recordings from saccade-related neurons in the deep cerebellar nuclei of monkeys (oculo-motor region of fastigial nucleus), we hypothesize that saccadic lateropulsion in lateral medullary infarction is essentially identical with cerebellar saccadic dysmetria and results from a disruption of afferent olivocerebellar climbing fibres that gives rise to functional disinhibition of the cerebellar cortex and to increased inhibition of the deep cerebellar nuclei.

Adult↗
PubMed1994

[Variants of Todd's paralysis: postictal apraxia and prolonged postictal hemineglect].

Todd's post-epileptic paralysis is a well-known complication after focal or generalized epileptic seizures. The underlying pathophysiology, however, is still unknown. Commonly, it is associated with a hemiparesis, usually lasting minutes or hours, rarely as long as two days, with subsequent complete remission. We report 2 patients with unusual and variant post-epileptic syndromes which have not been previously described in the literature: first, an ideomotor limb apraxia, and second, a severe hemineglect syndrome. Each syndrome lasted up to 70 hours after the seizure and was completely reversible.

Adult↗
PubMed1993

[Glucocorticoid monotherapy for Cogan syndrome?].

A 27-year-old woman suddenly developed persistent rotatory dizziness with unsteadiness on standing and walking, associated with symptoms relating to the autonomic nervous system, all signs and symptoms disappearing without treatment in 3 days. Ten days before this episode she had noticed progressive bilateral impairment of hearing accompanied by tinnitus. Caloric and audiometric tests confirmed bilateral impairment of the audiovestibular organ. A week later she also developed bilateral iritis and papillitis. The constellation of ocular and audiovestibular signs suggested Cogan's syndrome. Under high-dosage glucocorticoid treatment (initially 1,000 mg/d prednisolone intravenously for 3 days, then 100 mg/d orally in decreasing doses down to 10 mg daily) the ocular signs improved, but the bilateral hearing impairment persisted. A recurrence occurred after 5 months, while on a prednisolone dosage of 10 mg daily, together for the first time with arthralgias, suggesting systemic involvement. Although the symptoms quickly subsided when dosage was increased to 100 mg daily, repeated attempts at dose reduction brought about renewed exacerbation at 70 mg daily. As the necessary high steroid dosage led to severe side effects, an immunosuppressive drug was added (100 mg cyclophosphamide and 20 mg prednisolone, both daily; later 5 mg methotrexate weekly and 4 mg prednisolone every other day). The symptoms had not recurred when re-examined 7 months later.

Administration, Oral↗
PubMed1992

["Abducens neuromyotonia" with partial oculomotor paralysis].

Paroxysmal involuntary spasms of extraocular eye muscles which can lead to reversible pathological eye positions and limitations of eye movements are etiologically heterogenous. Despite the diagnostic difficulty, they are important as a neurological sign because of the usually good response to treatment. We report on a patient with the unusual combination of ocular neuromyotonia with brief paroxysmal tonic lateral deviation of the left eye and a concomitant partial third nerve palsy. The paroxysmal episodes disappeared with carbamazepine therapy. Possible pathomechanisms are discussed.

Abducens Nerve↗
PubMed1990

Spinal somatostatin superfusion in vivo affects activity of cat nociceptive dorsal horn neurons: comparison with spinal morphine.

A controversy exists concerning the role of the neuropeptide somatostatin for the transmission or inhibition of nociceptive information in the spinal cord. To better correlate electrophysiological effects of somatostatin at single cell level with results obtained with intrathecal injections of somatostatin in behaving animals and human pain patients we applied somatostatin to the spinal cord by controlled superfusion of the recording segment in vivo. The hypothesis of an opioid link and possible neurotoxic effects of somatostatin were also addressed. In cats deeply anaesthetized with pentobarbitone, halothane and nitrous oxide, extracellular recordings were made from 27 neurons located in laminae I-VI. All neurons responded to both innocuous mechanical and noxious radiant heat stimuli applied to the glabrous skin of the ipsilateral hindpaw. The dorsal surface of the spinal cord was superfused at the recording segment by means of a Perspex chamber (7 x 7 mm). Somatostatin superfusions at 1.2 microM had no effect on responses to noxious heat. Responses were, however, depressed by somatostatin at 61 microM to 59.7 +/- 5.1% of control and by somatostatin at 1.53 mM to 39.9 +/- 9.5% of control. This inhibition was not antagonized by the mu-opiate antagonist naloxone applied to the spinal cord at concentrations of 2.7 mM, either together with somatostatin, or after the inhibition by somatostatin had fully developed. Neuronal responses were linear functions of the skin temperatures for stimulation intensities between 42 degrees C and 52 degrees C. The slopes of these stimulus response functions were reduced during somatostatin superfusion at 61 microM to 46.8 +/- 9.3% of control, without changing the temperature thresholds for responding (42.5 +/- 0.6 degrees C). Somatostatin superfusion at 61 microM had no effect on the number of action potentials evoked by innocuous skin brushing, or by electrical stimulation of primary afferent A-fibres in cutaneous nerves. The amplitude of intraspinally recorded field potentials evoked by these electrical nerve stimuli was also unaffected by somatostatin. The inhibition of nociceptive spinal dorsal horn neurons by spinally administered morphine was assessed in eight experiments. Morphine reduced noxious heat-evoked responses to 42.1 +/- 9.6% of control at 0.3 mM and to 51.8 +/- 6.9% of control at 3.0 mM. The slopes of the stimulus-response functions were reduced by morphine at 0.3 mM to 53.1 +/- 11.3% of control, without changing the temperature thresholds (42.7 degrees C). Naloxone superfusion (2.7 mM) reliably antagonized the inhibition by morphine. Brush-evoked responses were not, or much less, affected by spinal morphine.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Inhibition of spinal nociceptive neurons by excitation of cell bodies or fibers of passage at various brainstem sites in the cat.

The relative contribution of cells of origin and fibers of passage to the inhibition of spinal nociceptive neurons from various brainstem sites is not known. The present study therefore quantitatively compares the descending inhibition produced by focal electrical stimulation which indiscriminatively excites all neuronal elements with the inhibition evoked by glutamate microinjections which selectively excite cell bodies at the same sites within the midbrain periaqueductal gray (PAG) and neighboring lateral reticular formation (LRF) and within the medullary nucleus raphe magnus (NRM). In pentobarbital anesthetized cats extracellular recordings were made from 22 lumbar dorsal horn neurons responding to innocuous mechanical skin stimuli and to noxious radiant heating of the glabrous skin at the ipsilateral hindpaw. Glutamate microinjections (1 microliter, 0.5 M) into 6 of 10 sites within the NRM reduced heat-evoked responses in 6 different cats to 69.2 +/- 3.8% of control. Electrical stimulation (180-600 microA) at the same sites and two additional sites in the NRM reduced responses to 50.0 +/- 8.7% of control. At 4 of 10 sites within the PAG glutamate reduced spinal neuronal responses to heat in 4 different cats to 69.4 +/- 6.1% of control. Electrical stimulation at 3 of the same sites and 6 additional sites within the PAG reduced heat-evoked responses to 52.7 +/- 3.5% of control. Microinjections of glutamate into the LRF failed to affect heat-evoked responses in any of the 8 experiments tested, while electrical stimulation at 6 of the same sites in the LRF reduced neuronal responses to heat to 52.4 +/- 7.1% of control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Pentobarbital, in subanesthetic doses, depresses spinal transmission of nociceptive information but does not affect stimulation-produced descending inhibition in the cat.

The present study evaluates the effect of systemic pentobarbital on the spinal transmission of nociceptive information and on stimulation-produced descending inhibition in the deeply anesthetized, paralyzed cat. Single neuronal responses to noxious skin heating were recorded extracellulary in the lumbar dorsal horn and found to be depressed by pentobarbital at subanesthetic doses (4.0, 8.0, 17.0 and 24.5 mg/kg) in a dose-dependent manner. At 0.5 and 1.5 mg/kg, depression by pentobarbital was positively correlated with the depth of the recording site in the spinal cord (laminae IV-VI), i.e., neurons in deeper laminae (V-VI) were attenuated, while neurons in lamina IV were unaffected. At all doses tested, pentobarbital failed to affect stimulation-produced descending inhibition from either the midbrain periaqueductal gray or the medullary nucleus raphe magnus. The present data furnish evidence for the antinociceptive potency of pentobarbital, they do not support the view that a 'partial pharmacological spinal cord transection' would attenuate stimulation-produced descending inhibition of nociceptive dorsal horn neurons.

Animals↗
PubMedDate not supplied

Bilateral loss of eighth nerve function as the only clinical sign of vertebrobasilar dolichoectasia.

The case of a 55-year-old female is presented, in whom first a loss of the vestibular and hearing function on the left side occurred with sudden onset, and 3 days later an additional loss of functions on the right side occurred. No other neurological symptoms were present. Angiography and MRI scan revealed vertebrobasilar dolichoectasia with a thrombus attached to the wall of the basilar artery. Anticoagulative therapy improved hearing function on the right side sufficiently to allow conversation. Vestibular organs remained unresponsive to caloric irrigation. This bilateral loss of eighth nerve function is discussed as a rare case of bilateral ischemia of the labyrinthine artery due to basilar dolichoectasia.

Aneurysm↗
PubMedDate not supplied

Saccadic dysmetria is similar in patients with a lateral medullary lesion and in monkeys with a lesion of the deep cerebellar nucleus.

Some of the clinical hallmarks of lateral medullary infarction--Wallenberg's syndrome--are saccadic dysmetria, smooth pursuit deficit, and lateropulsion of the body. Similar movement disorders are seen in monkeys after local unilateral injection of GABAergic drugs in the caudal fastigial nucleus of monkeys. These include an ipsilateral saccadic hypermetria and a contralateral saccadic hypometria as well as cogwheel smooth pursuit eye movements toward the contralateral side and an ipsiversive lateropulsion of the body. It was previously suggested that the lateral medullary infarction causes a lesion of climbing fibers to the cerebellum. This lack of climbing fiber input increases the activity of ipsilateral Purkinje cells, which consequently provide too much inhibition of the deep cerebellar nuclei.

Adult↗
PubMedDate not supplied

Cogan's Syndrome. High resolution MRI indicators of activity.

In the chronic-relapsing form of Cogan's syndrome, it can be difficult to evaluate the activity of the disease. In contrast to the initial stage, routine diagnostic techniques sometimes fail to indicate progression in the chronic stage. To determine whether high-resolution magnetic resonance imaging (HR-MRI) can be used to differentiate between active and inactive stages, we examined three patients with Cogan's syndrome (one during an acute relapse, two with chronic audiovestibular deficits), all of whom had antibodies to inner ear tissue (cochlea, vestibular labyrinth). Unenhanced T1-, T2, gadolinium-enhanced T1-weighted, and three-dimensional constructive interference in steady stage (CISS) images were used. Abnormal MRI signals of the inner ear were related to the activity of the disease. The patient studied during an acute exacerbation showed abnormal MRI signals in the vestibule, semicircular canals, vestibular nerve, and cochlea, which disappeared after the relapse. These abnormalities included high signal in the membranous labyrinth, the vestibule, and cochlea, with enhancement on T1-weighted images, indicating gadolinium leakage through the abnormal labyrinthine membrane into the perilymphatic spaces. In contrast, the other two patients with chronic audiovestibular deficits but no clinical signs of an acute relapse, had narrowing or occlusion of semicircular canals of the cochlea on the 3D-CISS images, but no high signal lesions (T1) and no enhancement. We conclude that sequential gadolinium-enhanced MRI can identify the active stage of Cogan's syndrome. The combination of HR-MRI and antibodies to inner ear antigens are helpful in the diagnosis of acute, sequential, bilateral audiovestibular impairment of autoimmune origin.

Acute Disease↗