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Biomedical subjects

P D Clouston

Publications and source records attributed to P D Clouston.

16 recordsLinked to original sources
PubMed2003

Sudomotor nerve conduction velocity and central processing time of the skin conductance response.

OBJECTIVE: To estimate the sudomotor nerve conduction velocity (CV), the central processing time (CPT) and habituation of the skin conductance response (SCR). METHODS: SCRs in response to a single deep inspiratory breath, an electrical stimulus and a sound click were obtained from the fingers and toes of 30 healthy adults. Sudomotor nerve conduction velocities were determined after measuring extremity length and latency differences. CPT was estimated by subtracting the efferent time and the known afferent times and neuroeffector times from the onset latency. RESULTS: The inspiratory SCR habituated slower than the auditory or electrical SCRs. CVs of the 3 modalities did not differ statistically and their mean was 1.07 m s(-1) (95% CI: 1.01-1.13). The inspiratory SCR arrived at the fingers 1.26+/-0.09 s after the onset of chest wall movement. Electrical and auditory SCR onset latencies at the fingers were 1.60+/-0.03 and 1.75+/-0.04 s, respectively. Their CPTs were 140 and 160 ms, estimated from the electrical and auditory SCR onset latencies to the fingers. The CPT for inspiratory SCR was estimated to occur during the inspiratory CPT after the inspiratory decision and before chest movement. CONCLUSIONS: In contrast to the SCR following an electrical or auditory stimulus, initiation of deep inspiratory SCR occurs before the inspiratory act, precluding any possible input from respiratory afferent receptors and implicating a central generator. SIGNIFICANCE: This study provides new insights into the origin of the SCR following inspiration.

Adult↗
PubMed2000

The current use of botulinum toxin.

Botulinum toxin is the most potent neurotoxin known, and has been in clinical use since the late 1970s. The toxin inhibits the release of acetylcholine from nerve terminals by inhibiting transport of the synaptic vesicles, thus causing functional denervation lasting up to 6 months. Our understanding of the mechanism of action of the toxin and the spectrum of diseases treatable with this agent continues to increase. Efficacy has been demonstrated in hemifacial spasm, dystonia, spasticity, hyperhidrosis and other conditions. Alternative serotypes are used in some centres, generally after the development of immunoresistance to the standard toxin (serotype A), and are likely to be in routine use in the near future. This paper reviews the history, pharmacology and current uses of botulinum toxin.

Animals↗
PubMed1997

Diabetic neuropathy after pancreas transplantation: determinants of recovery.

Although simultaneous pancreas and kidney transplantation (SPK) achieves normoglycemia and correction of uremia in type I diabetic patients with renal failure, little data are available on long-term outcome and clinical determinants of recovery of peripheral neuropathy. In this prospective study, 219 electrophysiological studies using a standardized protocol were performed before and up to 8 years after SPK in 44 patients. Nine control diabetic recipients with functioning kidney but nonfunctioning pancreas transplants were studied on 35 occasions. Patients were 38.5+/-7.9 years old (mean+/-SD) with pretransplant diabetes present for 25.2+/-7.6 years. Significant polyneuropathy (total nerve conduction scores [NCS] <-1.0) was present in 89% before transplantation, which correlated with body weight (r=0.628, P<0.001). Two distinct patterns of neurological recovery were observed after SPK. Conduction velocity (CV) improved in a biphasic pattern, with a rapid initial recovery followed by subsequent stabilization. In contrast, the recovery of nerve amplitude was monophasic, and continued to improve for up to 8 years. Initial improvement in NCS was primarily due to an increase in CV (P=0.002 vs. baseline), and was best in shorter and younger patients. Recovery of total NCS at 6 months after SPK, assessed by multivariate analysis, was least in obese recipients and when performed in patients who had started dialysis before SPK, and was associated with lower transplant kidney isotopic glomerular filtration rate and HLA mismatch (P<0.05 to 0.001). Subsequent improvement was associated with less severe initial neuropathy, smaller body weight, and longer duration of diabetes (P<0.01 to 0.001). Fasting hyperinsulinemia was associated with impairment of initial recovery and subsequent NCS after SPK, but was worse in the control group. Recovery of nerve action potential amplitudes was predicted by better initial amplitudes and HLA mismatch, lower body weight, and the use of nifedipine (P<0.05 to 0.001). Nifedipine was used for hypertension in 33% of SPK and was associated with better CV and amplitudes, particularly in the upper limbs, where there was less neuropathy. The use of angiotensin-converting enzyme inhibitors also appeared beneficial, but this was confined to the lower limbs. SPK resulted in a gradual, sustained, and late improvement in nerve action potential amplitudes, consistent with axonal regeneration and partial reversal of diabetic neuropathy. These data suggest that early transplantation of uremic diabetic patients before onset of severe neuropathy, minimizing obesity and optimizing renal transplant function, maximizes neurological recovery after SPK. Furthermore, the preliminary data support randomized clinical trials for evaluation of nifedipine and angiotensin-converting enzyme inhibitors in diabetic neuropathy.

Adult↗
PubMed1996

Brainstem myoclonus in a patient with non-dopa-responsive parkinsonism.

In the few reports where electrophysiologic techniques have been used to characterise stimulus-sensitive myoclonus in the setting of a parkinsonian syndrome, the origin of the myoclonus has usually been found to be cortical. We describe a patient with parkinsonism unresponsive to levodopa who had myoclonus that was both spontaneous and induced by somatosensory stimuli. In addition, autonomic symptoms and a marked sleep disturbance were present early in his illness. Results of electrophysiologic investigations including electromyography (EMG) studies, routine electroencephalography (EEG) recording, jerked locked back-averaging of EEG, and somatosensory evoked potentials were consistent with a brainstem origin for the myoclonic jerks. Following ipsilateral digital and supraorbital electrical stimulation, the earliest muscle activation occurred in the trapezius. An all-night sleep study showed frequent myoclonic jerks during sleep and markedly abnormal sleep architecture. We believe that this patient's myoclonus was related to pathologic changes in brainstem reticular nuclei that occurred as part of his disease process. To our knowledge, brainstem myoclonus has not been described as a feature of parkinsonian syndromes.

Brain Stem↗
PubMed1996

Apomorphine can increase cutaneous inhibition of motor activity in Parkinson's disease.

We studied the effect of non-nociceptive ipsilateral digital stimulation on EMG recorded from a small hand muscle before and after the administration of subcutaneous apomorphine in 6 patients with Parkinson's disease. All were receiving the drug to control ¿on-off¿ fluctuations in motor performance. Averaged rectified EMG was recorded from tonically contracted abductor pollicis brevis (APB) following index finger stimulation using a brief stimulus train. In 5 patients motor evoked potentials (MEPs) were also recorded from APB during tonic contraction. A conditioning stimulus train was applied to the index finger at intervals between 15 and 65 msec prior to the transcranial magnetic stimulus. After apomorphine administration the patient group showed a significant increase in both EMG and MEP inhibition induced by digital stimulation. In patients with Parkinson's disease who have marked motor fluctuations, the inhibitory response of upper limb motor neurones to low level digital cutaneous stimulation can be altered by dopamine agonists.

Aged↗
PubMed1995

Modulation of motor activity by cutaneous input: inhibition of the magnetic motor evoked potential by digital electrical stimulation.

We examined the inhibitory effect of a brief train of digital (D2) electrical stimuli at 4 times perception threshold on transcranial magnetic motor evoked potentials (MEPs) recorded from abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles ipsilateral to the side of D2 stimulation. We compared this to the inhibitory effect of ipsilateral D2 stimulation on averaged rectified EMG recorded at 10% maximum voluntary contraction and on F-responses and H-reflexes recorded from these same muscles. We also compared MEPs recorded following D2 stimulation just above perception threshold to MEPs following higher intensity D2 stimulation. As well, we assessed the effect of preceding D2 stimulation on MEPs recorded from a relaxed versus tonically contracted hand muscle. D2 stimulation elicited a triphasic response of modest MEP facilitation followed by inhibition and further facilitation. The duration and onset of MEP inhibition correlated with those of the initial period of rectified EMG inhibition, however, the magnitude of MEP inhibition was generally less than the magnitude of EMG inhibition, consistent with a greater inhibitory effect of digital afferents on smaller motor neurons. MEPs were not facilitated during the rebound of EMG activity (the E2 period) that usually followed the initial period of EMG inhibition (I1 period). The behavior of H-reflexes and F-responses following ipsilateral D2 stimulation suggested that inhibition of both EMG and MEPs is not mediated via presynaptic inhibition of Ia afferents, and that inhibition is augmented by descending rather than segmental input to spinal motor neurons. Tonic contraction of the target muscle during D2 stimulation decreased the inhibitory effect of the preceding digital stimulus possibly due to recruitment of larger spinal motor neurons less likely to be inhibited by cutaneous input.

Adult↗
PubMed1994

Quantitative analysis of the compound muscle action potential in early acute inflammatory demyelinating polyneuropathy.

We quantitated the size and configuration of compound muscle action potentials (CMAPs) in 266 nerves (66 median, 67 ulnar, 71 tibial and 62 peroneal) of 72 patients with acute inflammatory demyelinating polyneuropathy (AIDP) initially studied within 19 days of symptom onset. Results were compared with criteria for CMAP abnormalities, including criteria for abnormal negative peak duration and desynchronisation, derived from a control population of 50 median, ulnar, tibial and peroneal nerves. Other motor conduction abnormalities including minimal F response latency were also examined. We also analysed patterns of CMAP abnormality, peak disability and outcome for AIDP patients who had at least 3 motor nerves evaluated at first electrophysiologic study. Amongst AIDP nerves, low amplitude of the distal CMAP, usually with prolonged distal latency, was much more common than an abnormal fall in CMAP amplitude between stimulus sites. Using our CMAP criteria more than half of these low amplitude distal responses showed prolonged negative peak duration of desynchronisation or both, consistent with demyelination. Of the 47 AIDP patients who had 3 or more nerves initially studied, 37 (78.7%) had at least 1 motor nerve with a distal CMAP showing evidence of temporal dispersion. In addition, those with at least 75% of motor nerves showing a pattern of low amplitude of the distal CMAP without a further significant fall in amplitude between stimulus sites had greater peak disability and a poorer outcome. Assessment of temporal dispersion of the distal CMAP should be included in electrophysiologic criteria for acute demyelination. In addition, for some patients with AIDP patterns of CMAP amplitude abnormality amongst motor nerves are present early in the illness and may provide prognostic information.

Action Potentials↗
PubMed1992

The spectrum of neurological disease in patients with systemic cancer.

To ascertain the range of neurological problems in patients with systemic cancer, we prospectively evaluated neurological symptoms, neurological diagnoses, and primary tumors in all patients with a history of systemic cancer examined by the Department of Neurology at the Memorial Sloan-Kettering Cancer Center, from Jul 1, 1990, to Dec 31, 1990. Of the 815 patients seen for neurological symptoms, less than half (45.2%) had metastatic involvement of the nervous system. The three most common symptoms were back pain (18.2%), altered mental status (17.1%), and headache (15.4%). The most common neurological diagnosis was brain metastasis (15.9%), followed by metabolic encephalopathy (10.2%), pain associated with bone metastases only (9.9%), and epidural extension or metastasis of tumor (8.4%). Of 133 patients with undiagnosed back or neck pain, 44 (33%) had epidural extension or metastases from tumor and 40 (30%) had pain associated with vertebral metastases only. In 15 (11%) the cause for the back pain was unrelated to metastatic disease. Of 132 patients seen on initial consultation for altered mental status, metabolic encephalopathy was the major neurological diagnosis (80; 61%); 20 (15%) had intracranial metastases. Of 97 patients with undiagnosed headache, 59 (61%) had a nonstructural cause. Fifty-three of these patients had either migraine, tension headache, or headache related to systemic illness (e.g., fever, sepsis). These results indicate that even in patients with systemic cancer, a group particularly prone to developing neurological disease that can be diagnosed radiologically, the role of clinicians remains important in helping distinguish noncancer-related and nonmetastatic neurological problems.

Adult↗
PubMed1992

Paraneoplastic cerebellar degeneration. III. Cerebellar degeneration, cancer, and the Lambert-Eaton myasthenic syndrome.

We studied nine patients with a subacute onset of a pancerebellar syndrome. Six had known cancer (three small-cell carcinoma of the lung [SCLC], one metastatic small-cell carcinoma, one small-cell carcinoma of the prostate, and one non-Hodgkin's lymphoma). Six of eight who had neurophysiologic testing, including the three patients without detectable cancer, had coexistent Lambert-Eaton myasthenic syndrome (LEMS). In two of the patients, LEMS was discovered only by neurophysiologic testing. We looked for anti-Purkinje cell autoantibodies in all patient's sera and in four patients' CSF. We also looked for autoantibodies to voltage-gated calcium channels (VGCCs) in seven patients' sera and two patients' CSF, using the 125I-omega-conotoxin radioimmunoassay. We were unable to detect anti-Purkinje cell autoantibodies in any patients' serum or CSF. However, there were raised titers of anti-VGCC autoantibodies in five of seven patients' serum, including one patient with SCLC who did not have LEMS, and in the CSF of one of two patients. We conclude that the frequency of presentation of a pancerebellar syndrome with LEMS is higher than expected by chance and is usually associated with cancer. In some of these patients, LEMS may be clinically occult. The presence of LEMS and raised titers of anti-VGCC autoantibodies in some patients with subacute cerebellar degeneration is suggestive of an autoimmune etiology even though anti-Purkinje cell antibodies could not be detected. Anti-VGCC autoantibodies are not confined to LEMS. They may be found at high titer in CSF as well as serum.

Aged↗
PubMed1990

Perineural spread of cutaneous head and neck cancer. Its orbital and central neurologic complications.

The ability of cutaneous squamous cell carcinoma of the face to cause ophthalmoplegia or central nervous system dysfunction via perineural spread is not well recognized. Five patients presenting to a general neurology unit are described in whom partial or complete ophthalmoplegia developed following fifth and seventh cranial nerve involvement by cutaneous squamous cell carcinoma. Two patients subsequently developed a contralateral hemiparesis; and one, multiple cranial nerve palsies as the tumor spread centrally. Normal radiologic findings or complete healing of the primary skin lesion caused delay in the diagnosis in three of the patients. When ophthalmoplegia or central nervous system dysfunction develops as a consequence of perineural spread of cutaneous facial cancer, management is palliative.

Aged↗
PubMed1990

Eosinophilic meningitis: cause of a chronic pain syndrome.

Three tourists developed eosinophilic meningitis after visiting the Fijian Islands. Two had a severe and long lasting illness with chronic intractable pain. In one patient electrophysiological studies and MRI scan of the brain were abnormal and provided evidence of both radicular and cerebral parenchymal involvement by the most likely causative agent, Angiostrongylus cantonensis.

Adult↗
PubMed1989

Acute necrotising myopathy associated with amiodarone therapy.

We report a patient who developed an acute painful proximal myopathy associated with the use of amiodarone. The temporal course, the presence of amiodarone related hypothyroidism and neuropathy, as well as the patient's improvement on drug withdrawal were consistent with a drug reaction. Muscle biopsy demonstrated an acute necrotising myopathy. The mechanism for this reaction is unclear.

Acute Disease↗