Peter Lüdemann

Cervical artery dissection—clinical features, risk factors, therapy and outcome in 126 patients

Abstract.The highly variable clinical course of cervical artery dissections still poses a major challenge to the treating physician. This study was conducted (1) to describe the differences in clinical and angiographic presentation of patients with carotid and vertebral artery dissections (CAD, VAD), (2) to define the circumstances that are related to bilateral arterial dissections, and (3) to determine factors that predict a poor outcome. Retrospectively and by standardised interview, we studied 126 patients with cervical artery dissections. Preceding traumata, vascular risk factors, presenting local and ischemic symptoms, and patientoutcome were evaluated. Patients with CAD presented more often with a partial Horner’s syndrome and had a higher prevalence of fibromuscular dysplasia than patients with VAD. Patients with VAD complained more often of neck pain, more frequently reported a preceding chiropractic manipulation and had a higher incidence of bilateral dissections than patients with CAD. Bilateral VAD was significantly related to a preceding chiropractic manipulation. Multivariate analysis showed that the variables stroke and arterial occlusion were the only independent factors associated with a poor outcome. This study emphasises the potential dangers of chiropractic manipulation of the cervical spine. Probably owing to the systematic use of forceful neck-rotation to both sides, this treatment was significantly associated with bilateral VAD. Patients with dissection-related cervical artery occlusion had a significantly increased risk of suffering a disabling stroke.

Pneumonia in acute stroke patients fed by nasogastric tube

Background: Aspiration pneumonia is the most important acute complication of stroke related dysphagia. Tube feeding is usually recommended as an effective and safe way to supply nutrition in dysphagic stroke patients. Objective: To estimate the frequency of pneumonia in acute stroke patients fed by nasogastric tube, to determine risk factors for this complication, and to examine whether the occurrence of pneumonia is related to outcome. Methods: Over an 18 month period a prospective study was done on 100 consecutive patients with acute stroke who were given tube feeding because of dysphagia. Intermediate outcomes were pneumonia and artificial ventilation. Functional outcome was assessed at three months. Logistic regression and multivariate regression analyses were used, respectvely, to identify variables significantly associated with the occurrence of pneumonia and those related to a poor outcome. Results: Pneumonia was diagnosed in 44% of the tube fed patients. Most patients acquired pneumonia on the second or third day after stroke onset. Patients with pneumonia more often required endotracheal intubation and mechanical ventilation than those without pneumonia. Independent predictors for the occurrence of pneumonia were a decreased level of consciousness and severe facial palsy. The NIH stroke scale score on admission was the only independent predictor of a poor outcome. Conclusions: Nasogastric tubes offer only limited protection against aspiration pneumonia in patients with dysphagia from acute stroke. Pneumonia occurs mainly in the first days of the illness and patients with decreased consciousness and a severe facial palsy are especially endangered.

Prevalence of factor V Leiden mutation in young adults with cerebral ischaemia: a case-control study on 225 patients

Abstract Cerebral ischaemia in young adults is a well-recognised disease, and approximately half of the cases remain aetiologically unclear despite extensive investigations. Thrombophilias are known to cause a subset of ischaemic strokes in this population. The factor V Leiden (FVL) mutation, causing resistance to activated protein C, has recently been recognised as the most important genetic thrombophilia in the Western population. Carriers of this gene mutation have a sevenfold increased risk of phlebothrombosis. We undertook this study to evaluate whether the FVL mutation constitutes a risk factor for juvenile cerebral ischaemias. A total of 225 patients aged ≤ 45 years at onset of cerebral ischaemia and 200 age-matched healthy controls were investigated. The overall frequency of heterozygosity for the FVL mutation did not differ significantly between patients (8.4%) and controls [6.0%; odds ratio (OR) 1.4, 95% confidence interval (CI) 0.7–3.1]. In the subgroup of patients with cryptogenic cerebral ischaemia (n = 94), however, a significantly higher frequency of this gene defect (15.9%) was found compared with the controls (OR 3.0, CI 1.3–6.6). Further trends towards higher frequencies of the FVL mutation were found in patients with patent foramen ovale (OR 1.9), individual (OR 2.1) or family history of previous thrombembolisms (OR 2.0), and in those aged 25 years at onset of disease (OR 1.9, all not significant). In conclusion, the FVL mutation is not a risk factor for cerebral ischaemia of the young. However, our results suggest that this gene mutation plays an aetiological role in the subgroup of patients suffering from ‘cryptogenic’ ischaemic events.

Hypoglossal nerve palsy as complication of oral intubation, bronchoscopy and use of the laryngeal mask airway

Hypoglossal nerve injury is a recognized but rare complication of oropharyngeal manipulation during intubation, bronchoscopy and use of a laryngeal mask airway. We present 2 new cases of temporary hypoglossal nerve palsy after orotracheal intubation for general anesthesia. The relevant literature is reviewed and different hypotheses concerning the pathophysiological mechanisms of nerve damage are discussed.

The Association between Disease Severity and Sleep-Related Problems in Patients with Parkinson’s Disease

Although sleep-related problems are a frequent finding in patients with Parkinson’s disease (PD), the aetiology is still unknown. We examined the associations between disease severity, sleep-related problems and social status in 116 PD patients participating in the FAQT Study, a prospective, German cohort study evaluating determinants of quality of life in PD patients. 47.4% of the patients reported sleep onset difficulties, 26.7% sleep interruptions, 14.7% had five or more sleep-related events during the night and 71.6% showed symptoms of increased daytime somnolence. The disease severity was significantly associated with sleep-related events (p = 0.01), the depression score with sleep onset difficulties (p = 0.04), sleep interruptions (p = 0.01) and the levodopa dose (p < 0.01). We conclude that depressive symptoms and increasing levodopa doses in PD patients mainly cause sleep onset difficulties and sleep interruptions, while the severity of motor symptoms contributes to sleep-related events like sleep walking, heavy sweating and nightmares.

Tiagabine-related non-convulsive status epilepticus in partial epilepsy: three case reports and a review of the literature.

There have been several recent reports of non-convulsive status epilepticus during tiagabine therapy in patients with partial epilepsy. We report three cases where elevation of tiagabine dosage was followed by electroclinical features, or electroencephalographic features without clinical signs, of non-convulsive status epilepticus. Administration of clonazepam and/or discontinuation to tiagabine lead to complete remission. In one case after re-exhibition of tiagabine the EEG again showed rhythmic delta waves. We review the other cases reported so far and discuss the different pathophysiological hypotheses about the association in the light of new experimental data.

Temporal hypometabolism at the onset of cryptogenic temporal lobe epilepsy

Abstract. Most patients with intractable temporal lobe epilepsy (TLE) exhibit temporal glucose hypometabolism. The reasons for the development of this abnormality are as yet unclear. The current notion is that an initial injury causes seizures, which in turn give rise to hypometabolism. The aim of this study was to assess whether temporal reductions in glucose metabolism in non-lesional TLE are the result of repeated seizures or whether hypometabolism represents an initial disturbance at the onset of disease. Glucose consumption was assessed with fluorine-18 fluorodeoxyglucose positron emission tomography (18F-FDG PET) in 62 patients with cryptogenic non-refractory TLE in different stages of disease. Twelve subjects without neurological illness served as controls. Patients with onset of epilepsy at least 3 years prior to the PET scan were defined as having chronic TLE. Using this criterion, the whole patient cohort included 27 patients with de novo TLE and 35 patients with chronic TLE. The groups were matched for age and sex. The appearance of high-resolution magnetic resonance images of the brain was unremarkable in all patients. In the total cohort, number, duration and frequency of seizures had a significant relation to the magnitude of hypometabolism. Temporal hypometabolism was exhibited by 26 of the 62 patients (42%), including 8 out of 27 (30%) with newly diagnosed TLE and 18 out of 35 (51%) with chronic TLE. The disturbances were more extensive and more severe in patients with chronic TLE. It is concluded that temporal hypometabolism may already be present at the onset of TLE, but is less frequent and less severe in newly diagnosed than in chronic TLE. The metabolic disturbance correlates with the number of seizures. These findings suggest that an initial dysfunction is present in a considerable number of patients and that hypometabolism is worsened by continuing epileptic activity.

Axonal polyneuropathy in obstructive sleep apnoea

Chronic hypoxaemia in chronic obstructive pulmonary disease is a well known risk factor for polyneuropathy but the impact of intermittent hypoxaemia on peripheral nerve function has not been established so far. A case-control study was performed to evaluate the prevalence of polyneuropathy in obstructive sleep apnoea (OSA). Out of 24 patients with OSA, 17 (71%) had clinical signs of polyneuropathy versus seven (33%) out of 21 matched controls. The mean amplitude of the sural sensory nerve action potential was smaller in the OSA group than in the control group, indicating axonal nerve damage. The differences were significant and could not be attributed to other known risk factors for polyneuropathy. The severity of axonal damage in patients with OSA correlated with the percentage of the night time with an O2saturation below 90%. It is assumed that recurrent intermittent hypoxaemia in OSA is an independent risk factor for axonal damage of peripheral nerves.

Neurosarcoidosis: clinical experience and diagnostic pitfalls.

Objective: To describe a group of patients with neurosarcoidosis and to highlight diagnostic difficulties based on current diagnostic criteria. Methods: The patient database of a general neurological department was searched for patients with established or suspected diagnosis of neurosarcoidosis. Twenty-four patients were identified with definite (n = 3), probable (n = 10) and possible neurosarcoidosis (n = 10). History and clinical, laboratory and imaging data of patients with definite and probable neurosarcoidosis were analyzed. Results: Cranial nerve symptoms were a dominant clinical feature, with the optic nerve being affected most frequently. Cerebrospinal fluid pleocytosis was found in more than half of the patients. Intrathecal IgG synthesis and oligoclonal bands were less frequent. There was a wide array of MRI lesions in both groups. Chest X-ray was false negative in 2 of 5 patients who also underwent a thoracic CT. Therapy with prednisolone was initiated in all patients. After a median of 36 months, 6 of 8 patients with follow-up data of >24 months were still in remission. Aggravation of symptoms required therapy escalation in 2 patients. Conclusion: There is a wide range of clinical symptoms and test results in patients with ‘definite’ or ‘probable’ neurosarcoidosis. Because systemic involvement is a crucial diagnostic criterion, extensive medical work-up may be necessary. Prognosis under corticosteroid treatment may be better than previously thought.

Treatment for obstructive sleep apnoea: effect on peripheral nerve function

Background and objective: Obstructive sleep apnoea (OSA) is suggested to be associated with peripheral nerve damage. A case–control study was conducted to provide further support to this observation. In a longitudinal intervention study, it was examined whether treatment for OSA has a possible beneficial effect on peripheral nerve function. Methods: Participants were 23 patients with OSA and 23 controls matched for age and body mass index (BMI), all without any known cause of peripheral nerve damage. The sensory nerve action potential (SNAP) amplitudes of both sural nerves were determined. After 6 months of treatment for OSA, treatment compliance was evaluated and nerve conduction studies were repeated. Results: Patients with OSA had significantly lower mean (standard deviation) sural SNAP amplitudes than controls (6.3 (3.5) v 11.2 (5.0), p<0.001). Multivariate regression analysis including the variables age, BMI and Apnoea–Hypopnea Index (AHI) showed that both age (p<0.01) and AHI (p<0.05) were inversely related to the SNAP amplitude. On follow-up, the sural SNAP showed an increase of 2.6 mV on average (p<0.001). Multivariate regression analysis including the variables age, BMI, AHI, pretreatment SNAP and treatment compliance identified only treatment compliance as being significantly related to the SNAP increase (p⩽0.005). Conclusion: OSA is an independent risk factor for axonal dysfunction of peripheral sensory nerves. Impaired neural function is at least partly reversible with treatment for sleep apnoea.