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PubMed2006

Clinical phenotype of subjects with Parkinson's disease and orthostatic hypotension: autonomic symptom and demographic comparison.

The objective of this study was to characterize the phenotypic associations of orthostatic hypotension (OH) in Parkinson's disease (PD). One hundred fifty-nine subjects with PD underwent assessment including autonomic symptom severity scoring, disease-specific rating scales, and measurement of postural blood pressure response. Symptoms of autonomic impairment weakly correlated with disease duration and severity. A posture and gait instability (PIGD) motor phenotype was associated with greater severity of autonomic symptoms. Eighty subjects (50.3%) had OH. These subjects were older, more likely to be male, and taking larger doses of dopaminergic medications than those without OH. There was no difference in disease severity or duration between those with and those without OH. Symptomatic dizziness did not distinguish between groups, although subjects with OH had more symptoms of generalized autonomic impairment than those without. Progressive autonomic involvement may be linked to disease progression in PD, particularly in patients with a PIGD phenotype, but dichotomization into groups with and without OH is a relatively insensitive method for demonstrating this. Longitudinal studies of changes in autonomic reflex abnormalities, autonomic symptom profiles, and motor severity might clarify these associations.

Aged↗
PubMed1987

Increased shortening reaction in Parkinson's disease reflects a difficulty in modulating long loop reflexes.

Short and medium latency electromyographic (EMG) responses to stretch of the triceps surae muscle and long latency EMG responses (LL) in the anterior tibial muscle (TA) were evoked by toe-up tilt of a movable platform while standing or sitting, in normal subjects and patients with Parkinson's disease. With the stimulus parameters used (amplitude 4 degrees, velocity 50 degrees/s), LL in TA were absent in normals while sitting, but were present in 11 of the 12 patients with Parkinson's disease. In patients, LL latencies were identical in both positions. The results indicate that patients with Parkinson's disease have difficulty modulating long latency responses according to functional demands. Long latency responses in TA in the sitting position may correspond to the shortening reaction observed by others when much stronger stimuli were used.

Ankle Joint↗
PubMed1995

The audiogenic startle response in Tourette's syndrome.

We report the results of a study in which we examined the auditory startle responses (ASR) of 8 patients with Tourette's syndrome and 15 normal controls, none of whom reported or manifested exaggerated startle responses clinically. The ASR in two patients failed to habituate with repetition, a finding not present in any of the controls. There was no correlation between the presence or absence of exaggerated ASRs and the severity of the patients' tics. This study demonstrates that some patients with Tourette's syndrome have exaggerated audiogenic startle responses that may be clinically asymptomatic.

Acoustic Stimulation↗
PubMed1995

Saccadic eye movements in hyperekplexia.

Hyperekplexia is an autosomal dominant disorder characterized by excessive startle responses followed by a temporary generalized stiffness. The startle response is generated in the medial bulbopontine reticular formation in the lower brainstem. The pulse generator of horizontal saccadic eye movements is localized in the pontine paramedian reticular formation. Measurements of horizontal visually evoked random saccades, antisaccades, and saccades toward remembered targets were performed in seven patients with familial hyperekplexia and seven health age-matched controls. The peak velocity of all three kinds of saccades was reduced (p < 0.0001) compared with that of controls. Latencies were marginally longer in the patient group (p = 0.0486). Saccadic gains did not differ between patients and controls. The ability to make antisaccades, saccades toward remembered targets, and the ability to suppress reflex saccades are similar in patients and controls. These data suggest that the origin of the excessive startle response is probably more due to a different modulation in the brainstem than to altered cortical influence.

Acoustic Stimulation↗
PubMed1996

Brainstem encephalopathy with stimulus-sensitive myoclonus leading to respiratory arrest, but with recovery: a description of two cases and review of the literature.

Two unrelated patients developed bulbar symptoms, followed within several weeks by spontaneous myoclonus and painful, generalized, stimulus-sensitive jerks triggered by unexpected noises and cutaneous stimuli. They progressed to respiratory arrest and required mechanical ventilation, but both patients subsequently made an almost full recovery. These cases stress the importance of persevering with supportive treatment despite rapid progression of this severe generalized movement disorder. The relationship of brainstem reflex myoclonus to hyperekplexia, progressive encephalomyelitis with rigidity, and the stiff-man syndrome is discussed.

Adult↗
PubMed1992

Cutaneous reflexes in Parkinson's disease.

The physiology of rigidity in Parkinson's disease (PD) can be investigated by the study of reflexes. Cutaneous reflexes (CR) were measured in 10 patients with PD and in 10 age- and sex-matched normal volunteers. EMG activity was recorded from the first dorsal interosseous muscle with surface electrodes, rectified and averaged. The index finger was stimulated with an intensity four times the sensory threshold. The subjects abducted the index finger with 20% of maximal force. While the latencies of the different reflex components and the amplitudes of the excitatory peaks were not different in the two groups, the first inhibitory component was less pronounced in patients with PD as compared with normals. This effect is partially reversed with dopaminergic drug treatment. The results are compatible with the loss of an inhibitory spinal mechanism elicited by cutaneous afferents, and can be a partial explanation for increased tone in PD.

Electromyography↗
PubMed1996

The "muscle hypothesis" of chronic heart failure.

Chronic heart failure is a well-recognized syndrome in which left ventricular impairment produces a constellation of secondary changes in other organ symptoms leading to symptoms such as muscular fatigue and dyspnoea and objective limitation to exercise tolerance. With modern drug therapy of diuretics and ACE inhibitors, the majority of patients have minimal if any signs of congestion, and yet severe symptomatic limitation remains. This limitation bears little relationship to conventional measures of either left ventricular function or the haemodynamic profile of the patient. The symptoms limiting exercise are predominantly fatigue or dyspnoea, and yet the classical pathophysiological explanations for their genesis now seem inadequate. Recent investigations, as demonstrated, in part, by the research presented in this symposium, attest to the importance of abnormalities in peripheral blood flow and in skeletal muscle in producing both objective limitation to exercise and in explaining the generation of the exercise-limiting symptoms of the syndrome of stable optimally treated chronic heart failure. In addition it is now evident that these muscle changes may in addition have pathophysiological significance for the maintenance of sympatho-excitation during exercise and potentially therefore in the progression of left ventricular remodelling and in the susceptibility to ventricular arrhythmias. This paper presents some of the background evidence which leads to the hypothesis that a feedback loop links changes in skeletal muscle to abnormal reflex cardiopulmonary control which may both limit exercise and be harmful in the progression of the syndrome.

Cardiac Output, Low↗
PubMed1995

Murine leukemia virus-induced neurodegeneration of rats: enhancement of neuropathogenicity correlates with enhanced viral tropism for macrophages, microglia, and brain vascular cells.

A highly neuropathogenic retrovirus, NT40, was generated by serially passaging an infectious molecular clone of Friend murine leukemia virus, FB29, through F344 Fisher rats. NT40 induced severe neurological signs such as reflex abnormalities and ataxia within 4-6 weeks following neonatal inoculation. FB29 led to only very mild neurological dysfunctions with longer incubation periods. Pathological alterations were characterized by mild (FB29) to extensive (NT40) noninflammatory spongiform degeneration, mainly of brain-stem areas. Infectious center assays revealed that viral titers in brain tissues of NT40-infected rats were 100-fold higher than those of FB29-infected animals. Employing immunohistochemistry, in situ hybridization, and flow cytometry, NT40 was found to infect many endothelial cells of brain blood vessels and microglia, whereas FB29 infected only microglia and those to a lower extent. However, when isolated from adult diseased rats, microglial cells turned out in both cases to be nonproductively infected with either FB29 or NT40. Of peripheral organs, we found enhanced levels of NT40 in peritoneal macrophages but not in spleen, thymus, or serum when compared to FB29. Altogether these data suggest that an expanded cellular tropism within the CNS and elevated viral titers in macrophages and microglia correlated with enhancement of neuropathogenicity.

3T3 Cells↗
PubMed1976

[Paradoxical pupillary reaction to light -- a pupillographic study (author's transl)].

A report given of a 32-year-old female patient who exhibited a unilateral paradoxical pupillary reaction to light, but was obviously healthy in all other respects. All of the neuroophthalmological findings, including the infrared reflex-pupillographic results registered, are indicated and discussed in detail in the report. An analysis of the findings leads to the conclusion that this disturbance has a central, prenuclear location. Apart from a stenosis at the junction of the arteria vertebralis, which was determined angiographically, further examination did not reveal any pathological findings.

Adult↗
PubMed1976

Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention. II. Peripheral nerve disturbances.

80 strictly selected patients with chronic renal insufficiency with plasma creatinine values of 1.4-14.5 mg% were examined for clinical and electrophysiological signs of nephrogenic polyneuropathy. The motor symptoms complained of were cramps in 43.8% of the patients, "restless leggs" in 18.7%, muscular twitchings in 12.5%. It was emphasized that the first two symptoms do not always indicate the presence of polyneuropathy. 30% complained of paresthesias, 5% of "burning feet". The most frequent clinical finding was the impairment of vibration sense in the feet in 37.5% followed by diminshed appreciation of passive movement of the toes in 30%, weakening or absence of the ankle jerk in 23.8% and finally, weakening of the patellar reflex in 5%...

Adult↗
PubMed1983

The nosological position of Fisher's syndrome (ophthalmoplegia, ataxia and areflexia).

Fisher's syndrome was studied in six patients, one of whom was an 11-year-old girl, and the nosological position of this neuro-ophthalmological disorder was reviewed. The clinical features of the ophthalmoplegia in these cases were reported as secondary to a transient inflammatory lesion in the mid-brain; this was demonstrated in one of the cases by an enhancing area on CT scan. This mid-brain localization could explain not only the classical Fisher's triad but also many variations of the syndrome. The overlap of our cases of Fisher's syndrome with so-called brain-stem encephalitis of Bickerstaff has been emphasized. Many cases of Fisher's syndrome could therefore correspond to an inflammatory process at brain-stem level with or without nerve-root involvement. Clinical and neurophysiological findings show, however, that there is peripheral damage in some cases, so that a neutral attitude needs to be maintained on the nosological position of Fisher's syndrome.

Acute Disease↗
PubMed1986

Neuropharmacological investigations in the stiff-man syndrome.

In a patient with the stiff-man syndrome, abnormal exteroceptive reflexes in hand and arm muscles were used as a tool for investigating the effects of various centrally acting adrenergic drugs by means of acute testing. Clonidine, tizanidine and methamphetamine induced reflex suppression whereas reserpine had a biphasic effect: transient reflex suppression and delayed reflex enhancement. The drug actions on the reflexes paralleled to some degree those on the muscle stiffness. It is concluded that alpha-adrenergic stimulation leads to reflex suppression and muscular relaxation, whereas alpha-adrenergic blockade has the opposite effect. Correspondingly, long-term oral treatment with the alpha-stimulator, tizanidine, proved successful. The hypothesis is put forward that a noradrenergic system which exerts a net inhibitory influence on muscle tone and on exteroceptive reflexes plays an important role in the pathogenesis of the stiff-man syndrome.

Adrenergic Fibers↗
PubMed1991

Peduncular hallucinations.

Peduncular hallucinations usually present as visual disorders and are often genuine hallucinations associated with thalamic and/or mesencephalic lesions. In this case report we describe the clinical findings in a patient with hallucinations. Magnetic resonance imaging demonstrated bilateral ischaemic lesions in the thalamus and in the mesencephalon. The pathogenesis of hallucinations in these disorders is discussed in the light of the findings provided by imaging techniques.

Cerebral Infarction↗