Weight, body mass index (BMI) and energy expenditure/energy intake (EE/EI) was studied in 19 Parkinson's disease (PD) patients after subthalamic deep brain stimulation (STN-DBS) versus 14 nonoperated ones. Operated patients had a significant weight gain (WG, + 9.7 +/- 7 kg) and BMI increase (+ 4.7 kg/m2). The fat mass was higher after STN-DBS. Resting EE (REE; offdrug/ON stimulation) was significantly decreased in STN-DBS patients, while their daily energy expenditure (DEI) was not significantly different. A significant correlation was found among WG, BMI increase, and pre-operative levodopa-equivalent daily dose, their reduction after STN-DBS, and the differential REE related to stimulation and the REE in the offdrug/OFF stimulation condition. In conclusion, STN-DBS in PD induces a significant WG associated with a reduction in REE without DEI adjustment.
We assessed the usefulness of routine MRI for the differential diagnosis of Parkinson's disease (PD) with "atypical" parkinsonian syndromes in everyday clinical practice. We studied routinely performed MRI in PD (n = 32), multiple system atrophy (MSA, n = 28), progressive supranuclear palsy (PSP, n = 30), and corticobasal degeneration (CBD, n = 26). From a preliminary analysis of 26 items, 4 independent investigators rated 11 easily recognizable MRI pointers organized as a simple scoring system. The frequency, severity and inter-rater agreement were determined. The total severity score was subdivided into "cortical", "putaminal", "midbrain", and "pontocerebellar" scores. The frequency of putaminal involvement (100%) and vermian cerebellar atrophy (45%) was significantly higher in MSA, but that of cortical atrophy (50%), midbrain atrophy and 3(rd) ventricle enlargement (75%) was higher in PSP and CBD. The median total score fairly differentiated "atypical" parkinsonian syndromes from PD (positive predictive value-PPV-90%). However, the median total score was unable to differentiate atypical parkinsonian syndromes each other. The "cortical" score distinguished CBD and PSP from MSA with a fair PPV (>90%). The PPV of the "putaminal" score was high (70%) for the differential diagnosis of MSA with PSP and CBD. The "midbrain" score was significantly higher in PSP and CBD compared to MSA. These results are in accordance with the underlying pathology found in these disorders and demonstrate that a simple MRI scoring procedure may help the neurologist to differentiate primary causes of parkinsonism in everyday practice.
Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9·7 (SEM 7·1) kg after surgery, whereas patients on pharmacologic treatment lost 3·8 (SEM 10·0) kg since diagnosis. In STN-DBS-treated patients, REE (216·5 %; P,0·001), lipid oxidation (2 27 %; P, 0·05) and protein oxidation (2 46 %; P,0·05) were decreased, whereas glucose oxidation was elevated (þ81 %; P,0·05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (28·3 %; P,0·05) and glucose oxidation (2 37 %; P, 0·01) with a slight hyperglycaemic effect (after levodopa challenge: 5·6 (SEM 0·8) v. before levodopa challenge: 5·3 (SEM 0·6) mmol/l; P,0·01). Switching 'on' STN-DBS acutely reduced REE (217·5 %; P,0·01) and lipid oxidation (2 24 %; P, 0·001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5·4 (SEM 1·4) v. 5·5 (SEM 1·3) mmol/l; P,0·01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.
It has been suggested that the underactivity of mesial frontal structures induced by dopamine depletion could constitute one of the main substrates underlying akinesia in Parkinson's disease. Functional imaging and movement-related potential recordings indicate an implication of the frontal lobes in this pathological process, but the question has not yet been investigated at a cellular level using single unit recording. We therefore compared neuronal activity in both the presupplementary motor area (pre-SMA) and the supplementary motor area proper (SMAp) of the Macaca mulatta monkey during a delayed motor task, before and after MPTP treatment. In the pre-SMA, which receives strong inputs from the prefrontal cortex, the baseline firing frequency and the percentage of neurons responding to visual instruction cues decreased in lesioned monkeys. In the SMAp, which sends direct outputs to the primary motor cortex, not only was the response to visual cues impaired, but the percentage of SMAp neurons responding to intracortical microstimulation fell and the threshold of response rose. Neuronal activity after the Go signal diminished sharply in both structures in the symptomatic animal and the discharge pattern became more irregular; in the SMAp neuronal activity remained modified longer. Most of these changes could already be observed in the presymptomatic animal presenting no clinical signs of parkinsonism. These data would indicate that, at the moment when dopamine depletion has impaired the ability of cortical neurons to operate the focused selection of incoming information giving instructions for movement, pre-SMA and SMAp neurons are also in a state of severe hypoactivity. The conjunction of these phenomena could play a critical role in the genesis of akinesia.
Recent data suggest that a decreased basal ganglia output may occur in dystonia, resulting in an increased thalamic drive to the mesial premotor cortex. In a previous work we found that injection of the GABAA antagonist bicuculline into the rostral motor thalamus induced contralateral dystonic postures, whereas myoclonic jerks were frequent after injection into the caudal motor thalamus. In the present study, we performed electrophysiological recordings in the rostral and caudal parts of the ventrolateral thalamus of two cynomolgus monkeys before and after bicuculline injections or saline injections. Discharge frequencies of thalamic neurons were increased after bicuculline injections vs. controls. Their discharge pattern was more bursty in the caudal part in which bursts of neuronal activity were correlated with myoclonic jerks. After bicuculline injection, neurons responded more frequently and less selectively to passive limb movements in both parts of the motor thalamus. Conversely, the response to microstimulation increased after bicuculline injection, particularly in the caudal part. Our data show that acute bicuculline-induced dystonia is associated with a reversible overactivity and disorganization of neuronal activity in the motor thalamus. Such a phenomenon might induce an overspreading of cortical activity leading to dystonia. We postulate that the distinct clinical syndromes observed after bicuculline injections into the rostral and caudal motor thalamus are due to differences both in the neuronal circuitry within each thalamic nucleus and in segregated cortical projections.
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