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Biomedical subjects

H M Meinck

Publications and source records attributed to H M Meinck.

At least 19 recordsLinked to original sources
PubMed2007

[Myoclonus].

Myoclonus, an involuntary movement disorder reveals itself with a wide variety of short muscle twitches or jerks, and may cause severe disability. From a clinical perspective, it is sometimes difficult to discriminate myoclonus from other central movement disorders. Moreover, myoclonus has a spectrum of causes including rare neurological syndromes and uncommon manifestations of systemic disease. Its pathogenesis is only partially understood. Neurophysiologic investigations suggest a close relationship between certain types of myoclonic jerking and epilepsy. The use of anticonvulsants for treatment of myoclonus has its basis in such observations and empirical evidence. Often high doses or a combination of drugs, or both are required, with, however, serious side effects.

Anticonvulsants↗
PubMed2003

[Hepatic encephalopathy].

Hepatic encephalopathy (HE) is a neuropsychiatric complication of acute and chronic liver disease. Its etiology and pathogenesis are thought to be a complex, metabolically induced, and therefore potentially reversible disturbance in brain functions. The diagnosis is based on demonstrating both a disorder of the central nervous system and a concomitant liver disease as well as the exclusion of any neurological or psychiatric disorder of other etiology. The diagnosis of HE is clinical and displays a wide spectrum of neuropsychiatric symptoms in different degrees of severity. Ancillary diagnostic workup includes laboratory tests, neuroimaging, and neurophysiological exams such as electroencephalography and evoked potentials. The therapy of HE mainly consists of treatment and avoidance of any precipitating conditions such as high protein intake, infections, and gastrointestinal bleeding. Other therapeutic approaches modulate metabolic processes such as ammonium synthesis and excretion, formation of neurotransmitters, and as a last resort liver transplantation. The prognosis depends ultimately on the course of the liver disease.

Cerebral Cortex↗
PubMed2001

Masking of vertebral artery dissection by severe trauma to the cervical spine.

STUDY DESIGN: A prospective case study was performed. OBJECTIVES: To illustrate the association of cervical trauma with vertebral artery dissection, and to propose a diagnostic and therapeutic algorithm for suspected traumatic vertebral artery dissection. SUMMARY OF BACKGROUND DATA: Vertebral artery dissection is a recognized but underdiagnosed complication of trauma to the cervical spine. Symptoms of spinal cord injury, however, may obscure those of vertebral artery dissection, presumably causing gross underdiagnosis of this complication. METHODS: All patients with vertebral artery dissection admitted to the authors' facility between 1992 and 1997 were screened for cervical trauma. RESULTS: This article presents four patients with severe trauma to the cervical spine, defined as luxation, subluxation, or fracture, in whom symptoms of vertebral artery dissection developed after a delay ranging from several hours to weeks. The traumatic vertebral artery dissection typically was located at the site of vertebral injury or cranial to it. One patient with fracture of the odontoid process survived symptom free without ischemic brain infarctions. Another patient survived with traumatic quadriplegia in addition to large cerebellar and posterior cerebral artery infarctions. Two patients died as a result of fulminant vertebrobasilar infarctions, both with only moderate impairment from the primary spinal cord injury. CONCLUSIONS: Early signs of vertebral artery dissection include head and neck pain, often localized to the site of intimal disruption, which may be disguised by the signs of the spinal injury. Early Doppler ultrasound and duplex sonography as a noninvasive screening method should be performed for patients with severe trauma to the cervical spine. In cases of vertebral artery dissection, immediate anticoagulation should be initiated. Traumatologists should be aware of this complication in evaluating patients with severe trauma of the cervical spine, and also for a variety of forensic reasons.

Adult↗
PubMed2001

Interaction of tactile input in the human primary and secondary somatosensory cortex--a magnetoencephalographic study.

Interaction of simultaneous tactile input at two finger sites in primary (SI) and secondary somatosensory cortex (SII) was studied by whole-head magnetoencephalography. Short pressure pulses were delivered to fingers of the right and left hand at an interstimulus interval of 1.6 s. The first phalanx of the left digit 1 and four other sites were stimulated either separately or simultaneously. We compared four sites with increasing distance: the second phalanx of left digit 1, left digit 5, and digits 1 and 5 of the right hand. The temporal evolution of source activity in the contralateral SI and bilateral SII was calculated using spatiotemporal source analysis. Interaction was assessed by comparing the source activity during simultaneous stimulation with the sum of the source activities elicited by separate stimulation. Significant suppressive interaction was observed in contralateral SI only for stimuli at the same hand, decreasing with distance. In SII, all digits of the same and the opposite hand interacted significantly with left digit 1. When stimulating bilaterally, SII source waveforms closely resembled the time course of the response to separate stimulation of the opposite hand. Thus, in bilateral simultaneous stimulation, the contralateral input arriving first in SII appeared to inhibit the later ipsilateral input. Similarly, the separate response to input at two unilateral finger sites which arrived slightly earlier in SII dominated the simultaneous response. Our results confirm previous findings of considerable overlap in the cortical hand representation in SII and illustrate hemispheric specialization to contralateral input when simultaneous stimuli occur bilaterally.

Adult↗
PubMed2001

[Nocturnal spinal fracture--first manifestation of epilepsy].

A 54-year-old patient suffered overnight a double thoracic burst-fracture. One week later during the investigation for a metabolic or endocrinological cause, a witnessed seizure led to an unstable fracture of the humerus and the scapula. The neurological work-up revealed a cerebral astrocytoma as the epileptogenic focus. Forces generated during a tonic-clonic seizure can result in axial skeletal trauma, including thoracic and lumbar burst fractures. Vertebral fractures unrelated to an exogenous trauma are therefore always suspicious of an underlying epileptic disease.

Astrocytoma↗
PubMed2001

Hypoxic brain damage after intramuscular self-injection of diclofenac for acute back pain.

We present a case of hypoxic brain damage that occurred after intramuscular injection of diclofenac due to a severe anaphylactic reaction. A 38-year-old nurse treated herself for acute lower back pain with 100 mg diclofenac intramuscularly. Five minutes later, she collapsed and developed coma and respiratory arrest. After cardiopulmonary resuscitation she was transferred to hospital. On admission she was comatose and received controlled ventilation of the lungs. Magnetic resonance imaging and computerized tomography showed signs of hypoxic brain injury and the patient died from central cardiopulmonary failure 7 days later. Intramuscular treatment with non-steroidal anti-inflammatory drugs such as diclofenac has rare but potentially severe side-effects. Therefore, intramuscular injections are inappropriate and should be replaced with oral or rectal treatment, which has similar absorption profiles.

Acute Disease↗
PubMed2001

Antibodies against glutamic acid decarboxylase: prevalence in neurological diseases.

UNLABELLED: High prevalence of autoantibodies against glutamic acid decarboxylase (GAD-Ab) in stiff man syndrome (SMS) not only helps diagnosis, but also suggests immune mediated impairment of GABAergic functions. However, the presence of GAD-Ab has also been reported in other neurological syndromes. Therefore the prevalence of GAD-Ab was investigated in SMS, progressive encephalomyelitis with rigidity and myoclonus (PERM), and in other neurological diseases (OND). Serum antibodies against the GAD isoforms, GAD65 and GAD67, were investigated with radioimmunoassays in 13 patients with SMS, nine with PERM, 279 consecutive patients with OND, and in 100 normal controls. RESULTS: Prevalence of GAD65Ab was around 80% in patients with SMS/PERM compared with 5% in patients with OND and 1% in normal controls. Prevalence of GAD67Ab was 60% in SMS/PERM, 2% in patients with OND, and 1% in normal controls. Raised GAD-Ab clustered in an OND subgroup with sporadic progressive ataxia, but not in OND subgroups with recognised neuroimmunological diseases. In conclusion, increased GAD-Ab is neither a non-specific epiphenomenon of neuronal damage nor a common feature of recognised neuroimmunological disorders. In neurological diseases, GAD-Ab may be a pathogenetic agent or a marker for an ongoing autoimmune process, or both.

Antibodies↗
PubMed2001

Stiff man syndrome.

Stiff man syndrome (SMS), an uncommon neurological disease, is characterised by symmetrical muscle stiffness and spasms that often lead to skeletal deformity. Variants of the syndrome may involve one limb only (stiff leg syndrome), a variety of additional neurological symptoms and signs such as eye movement disturbances, ataxia, or Babinski signs (progressive encephalomyelitis with rigidity and myoclonus), or be associated with malignant disease (paraneoplastic SMS). Antineuronal autoimmunity and accompanying autoimmune diseases, most often insulin-dependent diabetes mellitus, are characteristic features of SMS and its variants. The condition is frequently misinterpreted as psychogenic movement disturbance, but electromyographic abnormalities and the presence of autoantibodies against glutamic acid decarboxylase (GAD) in both serum and cerebrospinal fluid help to establish the correct diagnosis. The aetiology of SMS is obscure. However, several features suggest that SMS is an autoimmune-mediated chronic encephalomyelitis. In line with this hypothesis, immunomodulation with a front-loaded methylprednisolone regimen reduces stiffness and spasms and improves other neurological symptoms in the majority of patients. Plasmapheresis or intravenous immunoglobulins are effective less frequently. For symptomatic treatment, the benzodiazepines are drugs of first choice. An alternative of last resort is baclofen administered intrathecally via an implanted pump device.

Animals↗
PubMed2000

Magnetic source imaging of tactile input shows task-independent attention effects in SII.

We investigated whether attention to different stimulus attributes (location, intensity) has different effects on the activity of the secondary (SII) somatosensory cortex. Tactile stimuli were applied to the left index finger and somatosensory evoked fields (SEFs) were recorded using a whole-head magnetoencephalography (MEG) system. Two oddball paradigms with stimuli varying in location or intensity were performed in an ignore and an attend condition. Brain sources were estimated by magnetic source imaging. No attention effect was observed for the primary SI area. However, attention enhanced SII activity bilaterally from 55 to 130 ms by 52% in the spatial and 64% in the intensity discrimination task. SII attentional enhancement was very similar in both paradigms and occurred both for deviants and standards.

Adult↗
PubMed2000

Gating of segmental and transcortical reflexes to human hand muscles depends on the mode of innervation.

We investigated the influence of the innervation pattern on the transmission of reflexes to a hand muscle. Reflexes were elicited by repetitive median nerve stimulation and recorded from the abductor pollicis brevis muscle. Both H and long loop reflexes were exclusively attenuated by irregular isotonic thumb abduction. In 10 of 15 experiments the long loop reflex was blocked completely. Inhibition intercalated between the H and long loop reflexes also decreased considerably. The observed attenuation of both spinal and supraspinal reflexes is suspected to take place mainly at the spinal level. Among the possible mechanisms, reciprocal inhibition is the most likely.

Adult↗
PubMed2000

Workshop I: Parkinson's disease and sleep--results of the group discussion.

The group agreed on the facts that unwanted sleep onset has been observed after non-ergot as well as ergot dopamine agonists, that patients on these drugs need to be warned, that patients who have experienced sleepiness already must not drive a car unless the dosage is lowered and sleepiness has vanished, that a genetic predisposition for narcoleptic cataplexy has to be ruled out, that predictors of so-called sleep attacks need to be explored individually with the help of sleepiness scales and collectively in a careful study, respectively.

Causality↗
PubMed2000

[Dystonia following peripheral trauma: clinical findings and diagnostic criteria].

Dystonia is a rare neurological complication after peripheral trauma. Incidence and pathophysiology of post-traumatic dystonia are not known. Predisposing factors are sympathetic reflex dystrophia, pre-existing movement disorders or a family history of movement disorders. The main diagnostic goal is to exclude other causes of secondary dystonia. Objective criteria for posttraumatic dystonia are not established, and therefore differentiation from psychogenic dystonia frequently remains difficult. Careful psychiatric examination is obligatory. Clinical criteria are consistency of the symptoms over time and the presence of symptoms compatible with organic dystonia. Polygraphic EMG examinations provide objective correlates of the movement disorder, but exact EMG criteria for the diagnosis of dystonia have yet to be established.

Adult↗
PubMed2000

Epitope spreading and a varying but not disease-specific GAD65 antibody response in Type I diabetes. The Childhood Diabetes in Finland Study Group.

AIMS/HYPOTHESIS: The aim of this study was to analyse the conformational and linear epitope profiles of glutamic acid decarboxylase antibody (GAD65-ab)-positive sera to find disease-specific epitope profiles and to study, whether GAD65-ab epitope recognition changes or spreads during the prediabetic period and, thus, can provide markers to differentiate early from later stages of progression to diabetes. METHODS: Sera from subjects before (n = 21), at onset (n = 44), or at increased risk of Type I (insulin-dependent) diabetes mellitus (n = 20) and from patients with stiff-man syndrome (SMS, n = 18) or polyendocrine autoimmune syndrome (PAS, n = 21) were analysed for conformational and linear GAD65 epitope recognition by an immunohistochemical blocking test based on human monoclonal GAD65-ab (MICA 1-10) and western blotting of a GAD65 epitope-cDNA-library. RESULTS: A redundant reactivity of many GAD65-ab positive sera to three major conformational (EP-1, EP-2, EP-3) and two dominant linear epitope clusters (amino acid 1-124 and 535-585) was observed in diabetes, polyendocrine autoimmune syndrome and stiff-man syndrome and no disease-specific epitopes or epitope-profiles were detected. Epitope recognition broadened with higher titres and with the vulnerability of patients to acquire additional autoimmune diseases apart from diabetes. Low GAD65-ab serum titres (< 1200 arbitrary units) and EP-1 recognition in the absence of EP-2 binding characterised the early immune response. Changing epitope profiles combined stable recognition of EP-1 with gain or loss of reactivity to C-terminal epitopes during follow-up. CONCLUSION/INTERPRETATION: A maturing autoantibody response, which could spread from EP-1-recognition to other regions of GAD65, resulted in titre-related rather than disease-specific epitope profiles which were not sufficient to predict whether GAD65-ab positive subjects will progress to Type I diabetes, autoimmune polyendocrine syndrome or stiff-man syndrome.

Adolescent↗
PubMed2000

The effect of changing stimulus intensities on median nerve somatosensory-evoked potentials.

We investigated median nerve somatosensory-evoked potentials (SEP) in 31 healthy volunteers to test the hypothesis that 1) increasing stimulus intensity influences SEP components in both amplitude and latency 2) SEP components respond differently to changing intensities. Cluster analysis and analysis of variance were used for statistical testing. Three groups of components could be found according to latency changes in response to increasing stimulus intensities: N13, and P15, the primary cortical response (N19, P22) and the components over 30 ms. In general, SEP components below 30 ms significantly shortened in latency and increased in amplitude with subsequent saturation. In contrast, in components over 30 ms latencies decreased linearly and amplitudes changed inhomogeneously. The clear effect of stimulus intensity on most median nerve SEP components makes it necessary to maintain comparable stimulus intensities when comparing intra- and interindividual registrations.

Adolescent↗
PubMed1999

The "CMT rat": peripheral neuropathy and dysmyelination caused by transgenic overexpression of PMP22.

We have generated a transgenic rat model of Charcot-Marie-Tooth disease type 1A (CMT1A) providing formal proof that this neuropathy can be caused by increased expression of peripheral myelin protein-22 (PMP22). Heterozygous PMP22-transgenic rats develop muscle weakness and gait abnormalities as well as reduced nerve conduction velocities and EMG abnormalities, which closely resemble recordings in patients with CMT1A. Dys- and demyelination, Schwann cell hypertrophy, and "onion bulb" formation are also similar to findings in humans. When bred to homozygosity, transgenic rats completely fail to elaborate myelin, but all myelin-forming Schwann cells segregate with axons in the normal one-to-one ratio. Although arrested at this "promyelin" stage, differentiation proceeds in homozygous rats at the molecular level, as demonstrated by high-level expression of myelin structural genes. Intracellular trafficking of the wild-type protein is not visibly impaired, even when strongly overexpressed, suggesting that PMP22 blocks myelin assembly in a late Golgi/cell membrane compartment of the affected Schwann cell.

Animals↗
PubMed1999

[Neuralgic neuropathies--complex pathogenesis and therapy. Trigeminal neuralgia--neuralgic shoulder amyotrophy--post-herpetic neuralgia].

A wide spectrum of manifestations and causes makes the diagnosis of neuralgic neuropathies difficult. In most cases, however, clinical and/or electrophysiological signs of a peripheral nerve disorder can be established. The pathomechanisms underlying pain are complex and not fully understood. They are not limited to the site of a lesion, but encompass the entire peripheral neurone, and may even involve the central neurones. Pathobiological correlates of chronic pain have been identified to involve the entire pain-mediating neuronal pathway.

Brachial Plexus Neuritis↗