Falls at advanced age - The importance to search for benign paroxysmal positional vertigo (BPPV).

INTRODUCTION: One of the most important geriatric syndromes is dizziness in conjunction with gait disorder and consequent falls. There are various differential diagnoses for dizziness, one of them is benign paroxysmal positional vertigo (BPPV). OBJECTIVES: A targeted diagnostic work-up and treatment of BPPV can prevent subsequent falls and a decline in the patients' quality of life, prolonged hospitalization with unnecessary examinations and medication. DESIGN: Prospective examination of patients with a positive medical history of BPPV. SETTING AND PARTICIPANTS: All patients treated within the Department of Geriatrics between 05/2015 and 03/2018 were included. A total of n = 5166 patients were screened (n = 2651 geriatrics; n = 2515 controls). METHODS: All patients from other wards subjected to a neurological examination due to vertigo served as controls. Patients with typical hints in the medical history for a BPPV were subjected to the diagnostic Dix-Hallpike maneuver and, if positive, subsequent canalith repositioning maneuvers. The percentage of successful positional treatments was determined in both groups. RESULTS: N = 254 patients (4.9 %) had indications in the medical history for a BPPV. For 71 of n = 254 patients (28 %; in total 1.4 %; mean age: 78.4 ± 12.3 years) the diagnosis of BPPV was proven by a positive Dix-Hallpike maneuver. N = 39 (54.9 %) patients belong to the geriatric group (mean age 82 years) and n = 32 (45.1 %) to the control group (mean age 73.9 years). The frequency of BPPV was similar in both groups (1.3-1.5 %). In 91.9 % of patients the BPPV was localized in the posterior semicircular canal. Up to 93 % were asymptomatic after one or repeated canalith repositioning maneuvers. CONCLUSIONS AND IMPLICATIONS: The BPPV should be considered as an important differential diagnosis for geriatric patients with dizziness and falls. After therapeutic repositioning maneuvers most of the patients are asymptomatic. Therefore, targeted screening and therapy ("theragnostic") of BPPV at an advanced age increases diagnostic accuracy and prevents unnecessary examinations, medications and future falls.

[Simvastatin-Induced Myopathy after Dose Increase]. / Simvastatin-induzierte Myopathie nach Dosiserhöhung.

HISTORY AND CLINICAL FINDINGS: We present a 86-year-old patient who suffered from progressive weakness in his right leg. Due to a hypercholesterinemia he had received Simvastatin for a few years. Because of higher cholesterine levels the dosis had been increased from 40 to 80 mg 6 months ago. INVESTIGATIONS AND DIAGNOSIS: We saw elevated levels of creatinine kinase and creatinine. In the EMG, a neuromuscular impairment was detected. In context with the medical history we could make the diagnosis of a statin-induced myopathy with rhabdomyolysis. TREATMENT AND COURSE: After stopping the medication with statin and under liquid substitution, creatinine kinase and creatinine levels dropped. After therapy the weakness of the leg was totally recurrent. CONCLUSION: In case of unclear neurological symptoms and under therapy with statins, a myopathy should be considered.

The Cologne stroke experience: safety and outcome in 450 patients treated with intravenous thrombolysis.

BACKGROUND: Predictors of outcome and safety in intravenous thrombolysis within 3 h in clinical routine is a matter of ongoing debate. Available reports contain small patient numbers or summarize heterogeneous multicenter data. METHODS: Four hundred and fifty patients received intravenous thrombolysis within 3 h after stroke. Pretreatment NIHSS score and detailed medical history were analyzed. Noncontrast CT was performed before thrombolysis, 24-36 h later and in case of clinical deterioration. Symptomatic intracranial hemorrhage (SICH; any bleeding with an NIHSS increase of > or =4 points) and clinical outcome (modified Rankin Scale, mRS) after 3 months were recorded. Logistic regression identified parameters predictive of independence (mRS 0-2) and SICH. RESULTS: Median onset to admission, door to needle and onset to treatment time was 75, 50 and 135 min, respectively. Direct presentation by emergency service (64%) was the fastest way of referral. Median pretreatment NIHSS was 11 points. Independence (mRS 0-2) was reached by 53%. Mortality was 11% (7% intracerebral, 4% extracerebral complications). Logistic regression identified low NIHSS, low age and absent diabetes as predictors of independence. Overall hemorrhagic complications and SICH were found in 18 and 4% of the patients, respectively. Extracerebral bleeding complications and allergic reactions were found in 3 and 1%, respectively. CONCLUSION: This largest single center report presents a sample in the range of the 3 h rt-PA cohort of all randomized controlled trials. Outcome was comparable to randomized studies with a higher rate of independence and a lower rate of mortality and SICH.

Early ischemic edema on cerebral computed tomography: its relation to diffusion changes and hypoperfusion within 6 h after human ischemic stroke. A comparison of CT, MRI and PET.

BACKGROUND: Brain tissue hypoattenuation on early computed tomography is frequently included in decision making in acute stroke management. However, its pathophysiological counterpart needs further evaluation. METHODS: By comparative imaging with diffusion-weighted imaging and 15O-water positron emission tomography we aimed to interpret early (<6 h) hypoattenuation. RESULTS: In 11 patients, the hypoattenuation corresponded to a decreased proton diffusion (median 115.9% relative DWI value) measured by magnetic resonance imaging and to a severe hypoperfusion (below 12 ml/100 g/ min) assessed by positron emission tomography. The volume of parenchymal hypoattenuation correlated to the tissue with disturbed diffusion (Spearman's rho=0.73), but largely underestimated the hypoperfusion below 20 ml/100 g/min. CONCLUSIONS: Early hypoattenuation reflects the coupling of the severity of ischemia and resulting diffusion changes. It allows an estimate of the infarct core but underestimates the penumbral hypoperfusion.