[Peripheral Nerve Injuries in Sports]. / Sportverletzungen peripherer Nerven.

Peripheral nerve injuries due to sports are relatively rare but the exact incidence is not known due to a lack of epidemiological studies. Particular sports activities tend to cause certain peripheral nerve injuries including direct acute compression or stretching, repetitive compression and stretching over time, or another mechanism such as ischemia or laceration. These nerve lesions may be severe and delay or preclude the athlete's return to sports, especially in cases with delayed diagnosis. Repetitive and vigorous use or overuse makes the athlete vulnerable to disorders of the peripheral nerves, and sports equipment may cause compression of the nerves. Depending on etiology, the treatment is primarily conservative and includes physiotherapy, modification of movements and sports equipment, shoe inserts, splinting, antiphlogistic drugs, sometimes local administration of glucocorticoids or, lately, the use of extracorporeal shock waves. Most often, cessation of the offending physical activity is necessary. Surgery is only indicated in the rare cases of direct traumatic nerve injury or when symptoms are refractory to conservative therapy. Prognosis mainly depends on the etiology and the available options of modifying measures.This article is based on the publications "Reuter I, Mehnert S. Engpasssyndrome peripherer Nerven bei Sportlern". Akt Neurol 2012;39:292-308 and Sportverl Sportschad 2013;27:130-146.

[Combination of two severe neurologic diseases--therapeutic dilemma with fatal outcome]. / Kombination aus zwei schweren neurologischen Krankheitsbildern--therapeutisches Dilemma mit fatalem Ausgang.

We present the case of a female patient with the combination of progressive cerebral sinus and venous thrombosis and unruptured intracranial aneurysm. Therapy of the symptomatic sinus thrombosis was initiated with heparin and endovascular occlusion of the aneurysm was planned within the next days. Before the coiling was performed fatal subarachnoid haemorrhage from the aneurysm occurred. The two dangerous neurologic diseases are presented and discussed with focus on symptomatology and therapeutic urgence.

Efficacy of natalizumab in second line therapy of relapsing-remitting multiple sclerosis: results from a multi-center study in German speaking countries.

BACKGROUND: Natalizumab has been recommended for the treatment of relapsing-remitting multiple sclerosis (RRMS) in patients with insufficient response to interferon-beta/glatiramer acetate (DMT) or aggressive MS. The pivotal trials were not conducted to investigate natalizumab monotherapy in this patient population. METHOD: Retrospective, multicenter study in Germany and Switzerland. Five major MS centers reported all RRMS patients who initiated natalizumab >or=12 months prior to study conduction. RESULTS: Ninety-seven RRMS patients were included [69% female, mean age 36.5 years, mean Expanded Disability Status Scale (EDSS) 3.4; 93.8% were pre-treated with DMT], mean treatment duration with natalizumab was 19.3 +/- 6.1 months. We found a reduction of the annualized relapse rate from 2.3 to 0.2, 80.4% were relapse free with natalizumab. EDSS improved in 12.4% and 89.7% were progression free (change of >or= 1 EDSS point). Eighty-six per cent of patients with highly active disease (>or= 2 relapses in the year and >or= 1 Gadolinium (Gd)+ lesion at study entry, n = 20) remained relapse free. The mean number of Gd enhancing lesions was reduced to 0.1 (0.8 at baseline). Discontinuation rate was 8.2% (4.1% for antibody-positivity). CONCLUSION: Natalizumab is effective after insufficient response to other DMT and also in patients with high disease activity.

Prevalence of migraine, tension-type headache and trigeminal neuralgia in multiple sclerosis.

BACKGROUND: Prevalence rates of headache in multiple sclerosis (MS) patients varied widely in recent studies. This study aimed to investigate the 1 year prevalence of headache in MS compared with the general population. METHODS: Population-based case-control study in Germany. RESULTS: We included 491 patients with definite MS (68% female, mean age 45.3 years, 63.7% relapsing remitting MS, mean Expanded Disability Status Scale (EDSS) 3.2, 106 treated with interferon-beta, 53 with glatiramer acetate, 271 untreated) and 447 age and gender matched controls. Headache was diagnosed with a validated questionnaire according to the International Headache Society Criteria. Headache prevalence was 56.2% (tension type headache 37.2%, migraine 24.6%). Headache prevalence rates did not differ from controls. Headache was not associated with disability or treatment. Trigeminal neuralgia was found in 6.3% of MS cases. CONCLUSION: Results suggest that headache in MS patients reflects comorbidity in most conditions.

[Therapy of myasthenia gravis]. / Die Therapie der Myasthenia gravis.

The treatment of myasthenia gravis is a difficult entity. We especially discuss the immunosuppressive treatment with regard to the literature. In patients with thymoma all authors agree in thymectomy. In generalized myasthenia, even without thymoma, thymectomy should be performed in "younger" patients. In "elderly" patients thymectomy as treatment of choice is controversial. The basis of immunsuppressive therapy are corticosteroids, additionally azathioprine can be given considering the delay in response and the major side effects. As today, cyclophosphamide and cyclosporine A are too toxic for routine use, except third choice in therapy resistant patients as ultima ratio. The procedure of choice in myasthenic crisis is plasma exchange if the patient tolerates it. Alternatively intravenous immunoglobulin should be given. In pure ocular myasthenia treatment is controversial in the literature. In the last few years there is a tendency to treat this form early like generalized myasthenia, especially in young patients, to prevent generalization.

Remission of severe alcoholic polyneuropathy after liver transplantation.

Alcoholic polyneuropathy presents with variable severity. Only few very severely disabled patients showed good clinical and electrophysiological improvement after cessation of alcohol abuse. We report a 55 year old patient with polyneuropathy who underwent orthotopic liver transplantation for decompensated alcoholic cirrhosis. After an initial postoperative exacerbation of her neurological disorder the patient developed an impressive remission of her clinical condition during the 4 year post transplantation follow up period. Nine months after surgery the initially wheel chair bound patient regained the ability to walk on her own. The previously severely impaired sensory modalities returned to nearly normal function. Electrophysiological findings also improved. The right tibial nerve conduction velocity increased from 16.8 to 26.7 m/s between the 27th and 37th post transplantation month. We postulate that liver transplantation facilitated the remission of this patient's alcohol-induced polyneuropathy. This observation suggests that alcoholic polyneuropathy, even when severe, should not be considered a contraindication for liver transplantation.

Postoperative brainstem and cerebellar infarcts.

OBJECTIVE: To study the clinical features and causes of postoperative brainstem and cerebellar infarcts. METHODS: Two groups were studied. The 10 group 1 patients had cardiac (eight) or aortic (two) surgery. The 12 group 2 patients had noncardiac-nonvascular surgery, including orthopedic (five), gynecologic (four), and general (three). Patients were studied by stroke services at university hospitals in Boston (13), Charlottesville (three), Baltimore (three), and Mainz (three) during 2 consecutive years. RESULTS: Onset of strokes was immediately postoperative (six), during the first 48 postoperative hours (nine), and delayed 3 days or more (seven). Clinical syndromes were altered level of consciousness or cognition (15), vestibulocerebellar (four), and hemiparesis with focal brainstem signs (three). Infarction involved the brainstem (13), cerebellum (13), and posterior cerebral artery hemispheric territory (10). Causes: In group 1, five infarcts were due to cardiogenic embolism and three to embolism from the aorta. One patient had a postoperative pontine lacunar infarct and one developed an infarct in the territory of a known stenotic basilar artery. In group 2, one patient had vertebral artery injury from instrumentation, one had medical complications with severe hemorrhage and hypotension, and 10 most likely had position-related vertebral artery thromboses. CONCLUSIONS: Patients with postoperative brainstem and cerebellar infarcts present with altered consciousness or vestibulocerebellar syndromes. The major cause of brain infarcts after cardiac surgery is embolism from the heart and aorta. The causes of infarction after general surgery are less clear, but neck positioning during or after surgery may play an important role by promoting thrombi in compressed arteries that later embolize intracranially when neck motion becomes free.

Prophylaxis and acute therapy of arterial embolism with special reference to cerebral embolism.

Prophylaxis and treatment of arterial embolism in high-risk patients includes therapy with antiplatelet drugs, anticoagulation, and vascular surgery. The prominent causes of cerebral ischemia are intraarterial emboli from atheromatous plaques and cardiac emboli. In patients with recent hemispheric transient ischemic attacks or minor stroke and ipsilateral high-grade internal carotid artery stenosis of 70 to 99% carotid endarterectomy has shown to be effective in prevention of major stroke or death. In the majority of patients with moderate atherosclerotic disease of the extracranial arteries as well as in patients with a cardiac source of emboli, no generally excepted therapy for primary and secondary prevention of cerebral ischemia or systemic embolism exists. The efficacy of antiplatelet drugs and anticoagulants in these patients is still investigated in a number of clinical multicenter studies. From the presently available data one can conclude that the antiplatelet agent acetylsalicylic acid in a dosage of 300 mg per day is effective in the secondary prevention of stroke and death in patients with preceding transient ischemic attacks, minor or major stroke and suspected artery-to-artery embolism from mild to moderate atherothrombotic carotid and vertebral artery disease. If there are no contraindications, we recommend anticoagulation in recurrent transient ischemic attacks not responding to antiplatelet drugs, in progressing stroke especially in the vertebrobasilar territory, in transient ischemic attacks in patients with rheumatic atrial fibrillation and left atrium thrombi, in minor stroke and proven cardiac embolism, in cerebral ischemia due to traumatic large vessel disease, and before and following elective cardioversion in patients with long-standing atrial fibrillation. A therapeutic dilemma still exists in patients with nonrheumatic atrial fibrillation; the presently available data are not sufficient to give recommendations whether aspirin or anticoagulants should be given for primary and secondary prevention of stroke and systemic embolism in these patients.

Polyneuropathy due to acute arsenic intoxication: biopsy studies.

A 41-year-old vintner attempting suicide ingested 8-9 g of arsenic and developed a symmetric polyneuropathy with acute Wallerian degeneration of myelinated fibers. Under treatment with modified British Anti-Lewisite (BAL; "Dimaval") his polyneuropathy slowly, but incompletely, subsided over three years at which time another sural nerve biopsy specimen showed regenerative proliferation of myelinated and unmyelinated axons but no signs of Wallerian degeneration. By laser microprobe mass analysis (LAMMA) arsenic was located in the first biopsied sural nerve specimen but not in the second specimen. These findings demonstrated: 1) arsenic induced serial morphometric and electron microscopic findings of nerve fiber degeneration and regeneration, 2) documentation of arsenic within myelinated nerve fibers, and 3) the usefulness of the LAMMA technique as a diagnostic procedure in this context.

Exophthalmos and basilar impression. A contribution to differential diagnosis of endocrine orbitopathy.

We report on a male patient with exophthalmos of unclear etiology, basilar impression, syringohydromyelia and type II Arnold-Chiari malformation. Two diseases involving the orbital region were to be considered in differential diagnostic terms: endocrine orbitopathy and osseous orbit dysplasia. The typical physical appearance associated with basilar impression as well as suppurative keratitis in Lagophthalmos was striking. Tetraspasticity with pareses, bulbar symptoms, proximally pronounced muscular atrophy as well as a left hemihypesthesia was shown neurologically. Although the orbit CT was normal, sonography revealed thickened ocular muscles. There was euthyroidism in diffuse goiter with negative thyroid autoantibody findings. Because of lack of definitive detection of muscular swelling, tumor, or vascular anomaly in the various images, orbital dysplasia in the context of a malformation syndrome affecting several organs is suggested as the cause of the exophthalmos.