Laboratory assessments in the course of Parkinson's disease: a clinician's perspective.

Physicians, caregivers and patients themselves must be alert to the onset of and changes in motor and non-motor features during the course of Parkinson's disease (PD). Parallel laboratory routine assessments are necessary because of the evolving impairment of the general health status of the individual. A number of potential biomarkers for the diagnosis of PD are currently under investigation, with diagnosis early in the disease course a particular goal, even before the onset of motor symptoms. The aim of this guideline article is to provide user-friendly, clinical evidence-based recommendations for using laboratory pathological testing for the diagnosis and differential diagnosis of PD, for assessing its time course, and managing complications of long-term dopaminergic therapy and the disabling motor features that develop in the later stages of the disease.

The Diagnosis and Treatment of Idiopathic Facial Paresis (Bell's Palsy).

BACKGROUND: Peripheral facial nerve palsy is the most com- mon functional disturbance of a cranial nerve. 60-75% of cases are idiopathic. METHODS: This review is based on a selective literature search proceeding from the current, updated German-language guideline on the diagnosis and treatment of idiopathic facial nerve palsy. RESULTS: The recommended drug treatment consists of prednisolone 25 mg bid for 10 days, or 60 mg qd for 5 days followed by a taper to off in decrements of 10 mg per day. This promotes full recovery (number needed to treat [NNT] = 10; 95% confidence interval [6; 20]) and lessens the risk of late sequelae such as synkinesia, autonomic disturbances, and contractures. Virostatic drugs are optional in severe cases (intense pain or suspicion of herpes zoster sine herpete) and mandatory in cases of varicella-zoster virus (VZV) infection. Corneal protection with dexpanthenol ophthalmic ointment, artificial tears, and a nocturnal moisture- retaining eye shield has been found useful in practice. In cases of incomplete recovery with residual facial weakness, both static and microsurgical dynamic methods can be used to restore facial nerve function. CONCLUSION: Because 25-40% of cases of facial nerve palsy are not idiopathic, differential diagnosis is very important; key diagnostic methods include a clinical neurological examin- ation, otoscopy, and a lumbar puncture for cerebrospinal fluid examination. High-level evidence supports corticosteroid treatment for the idiopathic form of the disorder.

Cerebellar speech representation: lesion topography in dysarthria as derived from cerebellar ischemia and functional magnetic resonance imaging.

BACKGROUND: Lesion topography and the pathophysiological background of dysarthria due to focal cerebellar lesions have not yet been fully clarified. OBJECTIVES: To investigate the lesion topography of dysarthria due to cerebellar ischemia and evaluate brainstem functions. DESIGN: Case studies. PATIENTS: Eighteen right-handed patients with sudden-onset dysarthria and cerebellar ischemia with and without brainstem involvement and 19 healthy, right-handed, monolingual, German-speaking volunteers. METHODS: In patients, we used multimodal electrophysiologic techniques to investigate brainstem functions. Functional magnetic resonance imaging (MRI) was performed in the 19 healthy volunteers. Activation tasks consisted of repetitive vertical silent movements of the tongue and lips at a self-paced rhythm. RESULTS: Cerebellar lesions and additional signs of brainstem involvement were observed in 11 patients with posterior inferior cerebellar artery, anterior inferior cerebellar artery, and superior cerebellar artery infarctions, respectively. In all other patients with isolated cerebellar infarction (n = 7), only the superior cerebellar artery territory (6 right-sided, 1 left-sided) was affected, and the common lesion site was the rostral paravermal region of the anterior lobe. Functional MRI in healthy volunteers indicated that the cerebellar representation of the tongue and orofacial muscles corresponds to that of the area involved in patients with cerebellar dysarthria. CONCLUSIONS: The results of this study demonstrate that articulatory movements of the tongue and orofacial muscles are involved in the activation of the rostral paravermal area of the anterior lobe. This location corresponds to the area involved in cerebellar ischemia in patients with dysarthria. Lesions in the upper paravermal area of the right cerebellar hemisphere, the site of coordination of articulatory movements of the tongue and orofacial muscles, may lead to the development of dysarthria that is unrelated to (often concomitant) brainstem infarctions.

Distribution and course of cortico-respiratory projections for voluntary activation in man. A transcranial magnetic stimulation study in healthy subjects and patients with cerebral ischemia.

The function and course of the cortico-respiratory projections in man are not yet well established. In 30 normal volunteers respiratory muscles were activated by magnetic stimulation of the motor cortex and the cervical and thoracic spinal roots with bilateral recordings from the respiratory muscles. Following cortical stimulation contralateral responses were obtained in all subjects during voluntary inspiration showing a mean latency and amplitude of 13.4+/-1.4ms/1.6+/-1.2 mV (stimulation of the left hemisphere) and 13.2+/-1.3ms/2.5+/-2.5 mV (stimulation of the right hemisphere). Ipsilateral responses were obtained in only 18 (right side) and 21 (left side) subjects and had a significantly (p < 0.001) longer mean latency and lower mean amplitude than the contralateral responses. In 31 patients with impairment of the cortico-respiratory projections due to cerebral infarction demonstrated by magnetic resonance imaging studies, the responsible lesion topography was analysed. We found that, 1. the voluntary activation of respiratory muscles is mediated predominantly by the contralateral motor cortex, 2. the descending cortico-respiratory projections are located within the pyramidal tract, and 3. the cortico-respiratory projections to the respiratory muscles are frequently affected in patients with hemiparesis due to acute stroke. These findings might explain the increased incidence of pneumonia at the hemiparetic side in patients with cerebral ischemia as shown in previous studies.