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Biomedical subjects

F Thömke

Publications and source records attributed to F Thömke.

At least 37 records · Page 2Linked to original sources
PubMed1999

Increased risk of sensory neuropathy in workers with chloracne after exposure to 2,3,7,8-polychlorinated dioxins and furans.

OBJECTIVE: The existence of a peripheral neuropathy after exposure to polychlorinated dioxins (PCDD) is still discussed, as studies concerning dioxin effects on the peripheral nervous system are rare and contradictory. MATERIAL AND METHODS: Clinical and neurophysiological examinations (motor conduction velocity of the peroneal nerve, sensory conduction velocities of the sural and ulnar nerves) were made in 156 dioxin exposed workers (42 with, 114 without cloracne) from one pesticide producing plant. Because of known risk factors for peripheral neuropathy, 7 workers with and 28 without cloracne were excluded from further analysis. RESULTS: Workers with chloracne had a significantly higher exposure against PCDD as documented by back calculated lipid levels. They complained significantly more often of sexual impotence (28.6% compared to 5.8% of workers without chloracne, P<0.001), had significantly more frequent clinical signs of a sensory neuropathy (= abnormal sensory findings plus deep tendon reflex abnormalities) restricted to the legs (17.1% compared to 1.2%, P<0.001), had significantly more frequent > or =2 neurophysiologic abnormalities (34.3% compared to 14.0%, P<0.025), and had significantly lower mean amplitudes of the motor compound muscle potential of the peroneal nerve. CONCLUSION: PCDD has a mild toxic effect on the peripheral nervous system manifesting as mild sensory neuropathy of the legs in a minority of the most severely exposed persons.

Acne Vulgaris↗
PubMed1999

Pontine lesions mimicking acute peripheral vestibulopathy.

OBJECTIVES: Clinical signs of acute peripheral vestibulopathy (APV) were repeatedly reported with pontine lesions. The clinical relevance of such a mechanism is not known, as most studies were biased by patients with additional clinical signs ofbrainstem dysfunction. METHODS: Masseter reflex (MassR), blink reflex (BlinkR), brainstem auditory evoked potentials (BAEPs), and DC electro-oculography (EOG) were tested in 232 consecutive patients with clinical signs of unilateral APV. RESULTS: Forty five of the 232 patients (19.4%) had at least one electrophysiological abnormality suggesting pontine dysfunction mainly due to possible vertebrobasilar ischaemia (22 patients) and multiple sclerosis (eight patients). MassR abnormalities were seen in 24 patients, and EOG abnormalities of saccades and following eye movements occurred in 22 patients. Three patients had BlinkR-R1 abnormalities, and one had delayed BAEP waves IV and V. Clinical improvement was almost always (32 of 34 re-examined patients) associated with improvement or normalisation of at least one electrophysiological abnormality. Brain MRI was done in 25 of the 44 patients and confirmed pontine lesions in six (two infarcts, three inflammations, one tumour). CONCLUSIONS: Pontine dysfunction was suggested in 45 of 232 consecutive patients with clinical signs of APV on the basis of abnormal electrophysiological findings, and was mainly attributed to brainstem ischaemia and multiple sclerosis. The frequency of pontine lesions mimicking APV is underestimated if based on MRI established lesions only.

Acoustic Stimulation↗
PubMed1999

Blink reflex R2 changes and localisation of lesions in the lower brainstem (Wallenberg's syndrome): an electrophysiological and MRI study.

OBJECTIVES: Pathways of late blink reflexes are detected by high resolution MRI. Electronically matched stroke lesions superimposed to an anatomical atlas show the suspected course. METHODS: Fifteen patients with infarction of the lower brainstem, MRI lesions and electrically elicited blink reflexes were examined. The involved structures in patients with R2 and R2c blink reflex changes were identified by biplane high resolution MRI with individual slices matched to an anatomical atlas at 10 different levels using digital postprocessing methods. RESULTS: The blink reflexes were normal in five of 15 patients (33%) and showed loss or delay of R2 and R2c to stimulation ipsilaterally to lesion (R2-i and R2c-i) in eight (53%). Loss or delay of R2-i/R2c-i was seen in lesions covering the entire trigeminal spinal tract and nucleus (TSTN) at at least one level. These infarctions were located more dorsally within the medulla. Patients with normal blink reflexes showed lesions sparing or involving the TSTN only partially. They more often had incomplete Wallenberg's syndromes and MRI lesions were located more ventrally. CONCLUSIONS: Using digital postprocessing MRI methods it was possible to identify central pathways of late blink reflex in patients with Wallenberg's syndrome. This method is suggested as a new approach to identify incompletely understood functional structures of the brainstem.

Aged↗
PubMed1999

Isolated cranial nerve palsies due to brainstem lesions.

Isolated cranial nerve palsies are often attributed to lesions of the respective nerves along their extraaxial courses. There are a significant number of reports of individual patients with cranial nerve palsies, mostly of the 3rd and 6th nerves, as the sole manifestation of brainstem lesions proven by magnetic resonance imaging (MRI) or computer-assisted tomography (CT). An intraaxial basis may still be underestimated if based on MRI only, as electrophysiological abnormalities indicating brainstem lesions (masseter reflex, blink reflex, DC electrooculography) may be independent from MRI-documented morphological lesions. This article reviews the evidence that ischemic and demyelinating brainstem lesions are an important and underestimated cause of clinically isolated cranial nerve palsies. Especially in middle-aged and elderly people with 3rd and 6th nerve palsies, small pontine and mesencephalic infarctions seem to be more frequent than small-vessel ischemic infarctions of the extraaxial nerves.

Aged↗
PubMed1998

Differentiation of recent and old cerebral infarcts by diffusion-weighted MRI.

We performed MRI, including diffusion-weighted imaging, in 15 patients with recurrent strokes with acute ischaemia and at least one old lesion according to the clinical history and/or CT. Routine MRI showed similar signal intensity changes in both situations. Diffusion-weighted images, however, were positive in all acute or subacute infarcts. The high signal of acutely disturbed diffusion due to intracellular oedema could also be identified in small brain stem lesions. Spatial resolution was increased by applying separate gradients in each axis instead of creating anisotropy-independent trace images.

Adult↗
PubMed1997

Evaluation of carpal tunnel syndrome in patients with polyneuropathy.

The difference between the median nerve latency to the second lumbrical muscle and the ulnar nerve latency to the second interosseous muscle (L-I DIFF) was tested in a prospective study to discriminate whether prolonged distal motor latency of the median nerve in patients with polyneuropathy (PNP) reflects an additional carpal tunnel syndrome (CTS). We investigated 92 patients (107 hands) with CTS, 30 patients (34 hands) with PNP, 22 patients (27 hands) with CTS and coexisting PNP (PNP + CTS), and 77 controls (87 hands). L-I DIFF was significantly prolonged in both the CTS and PNP + CTS patients as compared to PNP patients and controls. It proved to be the most specific test to differentiate between diffuse (PNP) and focal (entrapment) nerve disorder.

Adult↗
PubMed1997

Isolated cranial nerve palsies in multiple sclerosis.

During a 10 year period 24 patients with definite multiple sclerosis with isolated cranial nerve palsies were studied (third and fourth nerve: one patient each, sixth nerve: 12 patients, seventh nerve: three patients, eighth nerve: seven patients), in whom cranial nerve palsies were the presenting sign in 14 and the only clinical sign of an exacerbation in 10 patients. MRI was carried out in 20 patients and substantiated corresponding brainstem lesions in seven patients (third nerve: one patient, sixth nerve: four patients, eighth nerve: two patients). Additional abnormal findings of electro-oculography, or masseter reflex, or blink reflex, or combinations of these were found in 20 patients and interpreted in favour of a brainstem lesion at the level of the respective cranial nerve. In 11 of 14 patients with isolated cranial nerve palsies as the presenting sign of multiple sclerosis, dissemination in space was documented by MRI, and in the remaining three by evoked potentials. In patients with multiple sclerosis with isolated cranial nerve palsies, MRI is the most sensitive method of documenting dissemination in space and electrophysiological testing the most sensitive at disclosing brainstem lesions.

Adult↗
PubMed1995

Dissection of the internal carotid artery after chiropractic manipulation of the neck.

A 29-year-old woman died from a right hemispheric infarction caused by dissection and subsequent thrombosis of the internal carotid artery after chiropractic manipulations of the neck. Pathologic study of several arteries of muscular and elastic type revealed a mediolytic arteriopathy with widespread mucoid degeneration and cystic transformation of the vessel wall caused by segmental degeneration of smooth muscle cells of the tunica media. We hypothesize that mediolytic arteriopathy was a predisposing factor for the dissection of the internal carotid artery after chiropractic manipulations in our patient.

Adult↗
PubMed1992

[Localization of level of lesions in internuclear ophthalmoplegia through assessment of masseter and blink reflex].

The masseter and blink reflexes were investigated in 100 patients with internuclear ophthalmoplegia due to multiple sclerosis (58 patients) or lacunar brainstem infarction (42 patients). In unilateral internuclear ophthalmoplegia, 38 of 60 patients (63.3%) had masseter reflex abnormalities, two patients (3.3%) showed changes of the blink reflex R1 component, and 13 patients (21.7%) combined alterations of the masseter reflex and the blink reflex R1 component. 46 (86.8%) of these 53 patients with electrophysiological abnormalities had unilateral changes, which were ipsilateral to the medial longitudinal fasciculus lesion in 42 patients (91.3%). In bilateral internuclear ophthalmoplegia, 24 of 40 patients (60.0%) had abnormalities of the masseter reflex, two (5.0%) showed changes of the blink reflex R1, and nine (22.5%) combined alterations of the masseter reflex and the blink reflex R1 component. 20 (57.1%) of these 35 patients with electrophysiological abnormalities had bilateral changes. Thus, masseter reflex abnormalities indicating midbrain lesions were seen in 63.3% and 60.0%, respectively, of unilateral and bilateral internuclear ophthalmoplegia. Blink reflex R1 component changes with or without impairment of the masseter reflex indicating rostral pontine to midpontine lesions occurred in 25.0% and 27.5%, respectively. These figures correspond to the results of postmortem examinations and to theoretical considerations based on the length of the medial longitudinal fasciculus.

Adult↗
PubMed1992

Administration of tryptophan-enriched diets to pregnant rats retards the development of the serotonergic system in their offspring.

It is well established that an increased availability of tryptophan stimulates serotonin synthesis not only in the adult but also in the developing brain. In order to study the influence of a permanently increased supply of tryptophan on the developing central 5-HT-system, female rats were fed a tryptophan-enriched diet from mating throughout pregnancy and lactation. The effect of this dietary regime was assessed by measurements of neurochemical markers of 5-HT innervation in the developing brain of their offspring. A diminished content of 5-HT, a decreased activity of tryptophan hydroxylase and a reduction of crude synaptosomal high-affinity 5-HT uptake was found in the cortex and in the brain stem of 5 day old rat pups of mothers fed the tryptophan-enriched diet. The postnatal increase of all three markers of serotonergic innervation in the offspring of these mothers was retarded. Both the initial depletion and the delayed maturation of 5-HT content, of tryptophan hydroxylase activity and of synaptosomal serotonin uptake were more pronounced in the cortex than in the brain stem. Apparently, the increased dietary intake of tryptophan throughout pregnancy and lactation caused a delayed outgrowth of 5-HT axons and/or reduced collateral sprouting and synapse formation in the brain of the developing offspring.

Animals↗
PubMed1992

Acquired monocular elevation paresis. An asymmetric upgaze palsy.

Five patients with acquired monocular elevation paresis were investigated using direct current electroculography. With recovery, upward saccade velocities significantly increased in both eyes in all patients. The gain of upward-following eye movements significantly increased in the paretic eye of all patients and in the opposite eye of four patients. These findings are interpreted in terms of an asymmetric upgaze palsy which clinically presented as monocular elevation paresis in the more severely affected eye. A brainstem lesion contralateral to monocular elevation paresis was suggested in four patients by contralateral Horner's syndrome and contralateral abduction paresis, each in one patient, and contralateral ptosis in two patients. In only one patient, computerized tomography and magnetic resonance imaging substantiated a contralateral meso-diencephalic lesion.

Adult↗
PubMed1992

Abduction nystagmus in internuclear ophthalmoplegia.

Direct current electro-oculography revealed abduction nystagmus with hypermetric abduction saccades in 35 of 64 patients with unilateral and 55 of 66 patients with bilateral internuclear ophthalmoplegia. Slowing of abduction saccades occurred in 27 unilateral cases, mainly ipsilateral to the paretic eye, and in 36 bilateral cases. Abduction nystagmus with hypermetric abduction saccades of normal velocity is explained by an increased phasic innervation adjusted to adduction paresis. Slowed abduction saccades are attributed to impaired inhibition of the medial rectus muscle. Superposition of impaired medial rectus inhibition and increased phasic innervation best explains abduction nystagmus with slowed hypermetric (6 unilateral and 23 bilateral cases) or normometric abduction saccades (9 unilateral and 5 bilateral cases).

Adult↗
PubMed1992

Internuclear ophthalmoplegia of abduction: clinical and electrophysiological data on the existence of an abduction paresis of prenuclear origin.

Three patients showed unilateral and five bilateral abduction paresis. Five had associated adduction nystagmus of the contralateral eye. Electrophysiological testing of masseter and blink reflexes indicated an ipsilateral rostral pontine or mesencephalic lesion, and excluded a lesion of the infranuclear portion of the abducens nerve. Abduction paresis was attributed to impaired inhibition of the tonic resting activity of the antagonistic medial rectus muscle. The prenuclear origin of the disorder is based on morphological and neurophysiological evidence of an ipsilateral inhibitory connection between the paramedian pontine reticular formation and the oculomotor nucleus running close to but separated from the medial longitudinal fasciculus.

Abducens Nerve↗