MRI verified STN stimulation site--gait improvement and clinical outcome.

BACKGROUND: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is effective in alleviating Parkinson's disease (PD) symptoms (tremor, rigidity and bradykinesia) and may improve gait and postural impairment associated with the disease. However, improvement of gait is not always as predictable as the clinical outcome. This may relate to the type of gait impairment or localization of the active DBS contact. METHODS: The active contact was visualized on peri-operative magnetic resonance imaging in 22 patients with idiopathic PD, consecutively treated with bilateral STN DBS. Stimulation site was grouped as either in the dorsal/ventral STN or medial/lateral hereof and anterior/posterior STN or medial/lateral hereof. The localization was compared with relative improvement of clinical outcome (UPDRS-III). In 10 patients, quantitative gait analyses were performed, and the improvement in gait performance was compared with stimulation site in the STN. RESULTS: Of 44 active contacts, 77% were inside the nucleus, 23% were medial hereof. Stimulation of the dorsal half improved UPDRS-III significantly more than ventral STN DBS (P = 0.02). However, there were no differences between anterior and posterior stimulation in the dorsal STN. Step velocity and length improved significantly more with dorsal stimulation compared with ventral stimulation (P = 0.03 and P = 0.02). Balance during gait was also more improved with dorsal stimulation compared with ventral stimulation. CONCLUSIONS: Deep brain stimulation of the dorsal STN is superior to stimulation of the ventral STN. Possible different effects of stimulation inside the nucleus underline the need for exact knowledge of the active stimulation site position to target the most effective area.

Cued and non-cued repetitive ballistic movements. A kinematic study in healthy subjects.

Repetitive ballistic movements of the upper limbs were registered in 63 healthy subjects with an optoelectric 3-dimensional infrared computerized system. For evaluation of externally cued movements the arm was moved at maximum speed between two targets. As internally cued movements elbow flexion and extension at maximum speed was performed. At non-cued movements the subject shifted the hand between pronation and supination as fast as possible without further instructions. Movement velocity decreased progressively with increasing age at an annual rate of 0.5-0.6%. Women moved more slowly than men during cued movements, whereas no sex differences were found for non-cued movements. The peak velocity of cued movements remained unchanged during the 20 s performance period, whereas non-cued movements showed signs of fatigue with slowing. In conclusion, the maintenance of velocity during simple repetitive ballistic movements in healthy subjects depends on cueing and on sensory-motor function rather than on cognitive motor processing.

Initial sensorimotor and delayed autonomic neuropathy in acute thallium poisoning.

In a 27-year old male with acute thallium poisoning, signs of initially severe sensorimotor neuropathy with complete remission after two weeks were demonstrated. Signs of cardiovascular autonomic neuropathy were initially absent, but developed after a latency period of one week with marked improvement after seven months. Delayed autonomic neuropathy may be caused by a late affection of small unmyelinated autonomic nerve fibers.

Disordered mobility of large joints in association with neuropathy in patients with long-standing insulin-dependent diabetes mellitus.

Movement performance was studied in 29 long-term patients with insulin-dependent diabetes mellitus (IDDM) and 29 matched control subjects. Velocity, range of motion, reaction time, and strength of ankle dorsal and plantar flexion and knee extension were measured. The neuropathic condition was assessed from clinical examination, nerve conduction studies, and quantitative sensory examination, and summed to obtain a neuropathy rank-sum score. Reaction time for the diabetic patients was increased by 29%, 23%, and 22% for ankle dorsal, ankle plantar, and knee extension movements respectively (p < 0.001). Range of motion was slightly decreased at ankle dorsal flexion (12%, p < 0.05). There was an inverse relationship between range of motion and neuropathy rank-sum score for ankle dorsal (r = -0.68, p < 0.001) and plantar flexion (r = -0.61, p < 0.001). Peak velocity was significantly decreased at ankle dorsal (21%, p < 0.001) and plantar flexion (23%, p < 0.001) and was related to the isokinetic muscle strength. Peak velocity was also related to the neuropathy rank-sum score at ankle dorsal flexion (r = 0.57, p < 0.002). We conclude that maximal movements at the ankle are delayed and slowed in long-term IDDM patients. The decreased peak velocity and the range of motion are related to the severity of neuropathy.

Effects of dextropropoxyphene on the steady-state kinetics of oxcarbazepine and its metabolites.

The effects of dextropropoxyphene on the steady-state kinetics of oxcarbazepine and its metabolites were investigated in eight patients with epilepsy or trigeminal neuralgia. One patient dropped out of the study, presumably due to side-effects of dextropropoxyphene. Dextropropoxyphene did not affect the plasma levels of the principal active metabolite, 10,11-dihydro-10-hydroxy-carbamazepine. Since dextropropoxyphene is known to increase the plasma levels of carbamazepine, leading to toxicity, the findings of this study suggest that oxcarbazepine is a useful alternative to carbamazepine when concomitant dextropropoxyphene therapy is required.

Histopathology of anterior parts of the optic pathway in patients with multiple sclerose.

Multiple sclerosis involves the anterior part of the optic pathway of 5 patients with clinically definite multiple sclerosis. No pathological changes were found in the retina. Plaques were found in all optic nerves, in two of three chiasms and in the optic track from one patient. Periphlebitis was found in three optic nerves, and in one chiasm. One patient had plaques as well as periphlebitis in the optic nerves and chiasm but did not show any changes in the brain or the spinal cord.