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Objective: To describe the heterogeneity of electrodiagnostic (EDx) studies in Guillain-Barre syndrome (GBS) patients collected as part of the International GBS Outcome Study (IGOS). Methods: Prospectively collected clinical and EDx data were available in 957 IGOS patients from 115 centers. Only the first EDx study was included in the current analysis. Results: Median timing of the EDx study was 7 days (interquartile range 4-11) from symptom onset. Methodology varied between centers, countries and regions. Reference values from the responding 103 centers were derived locally in 49%, from publications in 37% and from a combination of these in the remaining 15%. Amplitude measurement in the EDx studies (baseline-to-peak or peak-to-peak) differed from the way this was done in the reference values, in 22% of motor and 39% of sensory conduction. There was marked variability in both motor and sensory reference values, although only a few outliers accounted for this. Conclusions: Our study showed extensive variation in the clinical practice of EDx in GBS patients among IGOS centers across the regions. Significance: Besides EDx variation in GBS patients participating in IGOS, this diversity is likely to be present in other neuromuscular disorders and centers. This underlines the need for standardization of EDx in future multinational GBS studies.(c) 2022 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Epidemics and pandemics in human history are not the exception but the rule. Bill Gates was prophetic in 2015 ‘if anything kills ten million people in the next few decades, it is likely to be an infectious virus rather than a war. Not missiles, microbes’. The Black Death (1347), the Great Plague of London (1665) and the Spanish Flu outbreak which killed 50 million people occurred in 1918. In 1997, the H5N1 bird flu epidemic occurred and was followed, in 2002, by the coronavirus outbreaks of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012. These were followed by the re-emerging pathogen epidemic; Ebola virus, unexpectedly, exploded in West Africa in 2013. While the world was celebrating the success of victory over Ebola, in 2015, the Zika epidemic reared its head. Significant neurological complications only featured in the Zika outbreak: congenital microcephaly, Guillain-Barre syndrome, myelitis and meningoencephalitis.1 The most well-studied coronavirus is the betacoronavirus, mouse hepatitis virus, that has provided model systems for the study of encephalitis and multiple sclerosis. In humans, coronaviruses usually cause common cold symptoms. However, the emergence of two zoonotic betacoronaviruses, SARS-CoV and MERS-CoV, revealed their full pathogenic potential.2 In December 2019, Zhu et al 3 described patients with pneumonia epidemiologically linked to a seafood and wet animal market in Wuhan, China. A novel coronavirus, SARS-CoV-2, was identified. WHO labelled the disease as COVID-2019. Further genomic analysis reveals that SARS-CoV-2 is similar to the betacoronavirus detected in bats but is a distinctly separate clade from SARS-CoV and MERS-CoV. A metallopeptidase, angiotensin-converting enzyme 2 (ACE2), has been identified as the functional cellular …

Our objective was to evaluate whether IV immunoglobulin (IVIg) increases the risk of thromboembolic events in neurology outpatients with inflammatory neuropathies, as there is conflicting evidence supporting this hypothesis, mainly from non-neurologic cohorts. We investigated this question over 30 months in our cohort of patients with inflammatory neuropathies receiving regular IVIg and found a greater incidence of arterial and venous thromboembolic events than population-based rates determined by hospital admissions data. Vascular risk factors were more common in the event group but there were no IVIg administration factors that contributed to the risk. This study suggests that IVIg may have a small but contributory role in determining thromboembolic risk in the inflammatory neuropathy cohort and more evidence is required before it is clear whether the current primary prevention guidelines are appropriate in this group of patients.

IntroductionHistorically, single tissue vasculitis has been managed with steroid monotherapy. Recent data from large longitudinal databases on systemic vasculitis suggest Non-Systemic Vasculitic Neuropathy (NSVN) has higher rates of relapse, recommending that more aggressive immunotherapy is employed.AimTo investigate the relapse rate in NSVN in response to steroid monotherapy.MethodsA retrospective case note review of clinically and/or pathologically defined cases of (Systemic Vasculitic Neuropathy) SVN and NSVN in two London specialist peripheral nerve centres, between 2005- 2012 and 2015 - 2019.Results32 cases of SVN and 34 cases of NSVN were identified. In each group 14 individuals were treated first-line with steroid monotherapy, and 8 with cyclophosphamide. 8 SVN and 9 NSVN cases received steroids plus azathioprine. 15/32 SVN and 13/34 NSVN relapsed after first-line therapy (10/14 and 9/14 on steroid monotherapy, 3/8 and 3/9 on steroids and azathioprine, 2/8 and 1/8 on cyclophosphamide). 10 individuals stabilised with the addition of azathioprine, 13 with cyclophosphamide and 4 with Rituximab.ConclusionThis representative case series suggests that steroid monotherapy is inadequate in the treatment of NSVN and supports an approach akin to that recommended in SVN, even if nerve is the only tissue clinically involved.e.bunting@nhs.net

A 67-year-old right-handed man who worked as a shipping merchant was brought to medical attention by his wife in May 2011. Although born and brought up in Scotland, he was at the time living alone in South Korea; he had last seen his family in January 2011, when he was well. His wife kept in daily contact with him, and in March 2011 she noted he was occasionally forgetful, for example, mixing up friends’ names. This progressed and by May 2011 he was losing his way home from work, prompting her to visit him. In addition to the cognitive symptoms, she noted he was eating little and had an unsteady gait. He was assessed in Seoul, where a new diagnosis of type 2 diabetes mellitus was made. He had a normal CT scan of head, and his gait was attributed to a diabetic peripheral neuropathy. He returned to the UK and attended clinic in May 2011. He could give a reasonable history and had a mini-mental state examination score of 26/30. He had been previously well, took no medications and had no relevant family history. He was an ex-smoker of 26 pack-years and drank in moderation. Before moving to Korea he had worked in the Merchant Navy, mainly in Asia. On examination, his gait was unsteady and he had signs consistent with a peripheral neuropathy, with reduced sensation in a glove and stocking distribution, and reflexes diminished in the arms and absent in the legs. Outpatient investigations were organised, but 2 weeks later his general practitioner requested admission due to a marked deterioration. On admission, his Addenbrooke's cognitive examination (revised) (ACE-R) was 51 (attention and orientation 7/18, memory 6/26, language 21/26, fluency 9/14 and visuospatial 8/16) with confabulation noted. The general examination was normal. The neurological examination showed an ataxic gait, …

Objectives? To describe the prevalence of distal sensory polyneuropathy (DSP), a complication of both advanced HIV disease and of antiretroviral therapy (ART), amongst Tanzanians with HIV, on and off ART (including stavudine) with CD4 counts above and below 200?cells/?l. Methods? We recruited participants attending ART clinic into four groups: >6?months ART exposure and (i) CD4? ?200?cells/?l (ART/CD4? ?200, respectively); ART-nai?½ve and (iii) CD4? ?200?cells/?l (noART/CD4? ?200, respectively). Primary outcome was DSP, as defined by presence of at least one symptom and one sign. Results? Of 326 evaluable participants, 81 (32 men, median age 38?years, median CD4 142?cells/?l) were enrolled in the ART/CD4? ?200, 81 (30 men, median age 37?years, median CD4 128?cells/?l) in noART/CD4? ?200. Numbness was the most commonly reported symptom. DSP prevalence ranged from 43.2% in ART/CD4? ?200. DSP was more common among men (adjusted odds ratio [aOR] 1.9, 95% confidence interval [CI] 1.2-3.3) and older participants (aOR 2.7, 95% CI 1.1-6.2 for age 40?+?vs.

ObjectivesTo improve the outcome of encephalitis in the region.DesignService evaluation of the introduction of monthly encephalitis meetings attended by specialist neuroradiologists, neurologists and infection doctors.SubjectsPatient referred at the discretion of the clinician from local hospitals and the tertiary referral centre.MethodsDiagnosis confirmed at the MDT or as a direct result of the MDT discussion.ResultsTo be presented.ConclusionsEncephalitis is a rare and complex clinical syndrome that requires close communication between neurologists and infection doctors. Setting up an MDT established this interaction, and streamlines patient care. Further, it provides access to novel technologies such as metagenomic diagnostic approaches.

Neurological complications of haematological malignancies are wide ranging but isolated myopathy as a presenting complaint is rare.Cases: 63 year-old lady with progressive proximal upper then lower limb weakness over 7 years to wheelchair-dependence and hoist-transfers. Muscle biopsy revealed nemalin rods, HIV negative, IgG kappa paraprotein=6 g/L. Late-onset nemalin rod myopathy was diagnosed; function is stable 6/12 post-autologous bone marrow transplant.56 year-old lady with limb-girdle weakness leading to immobility over 2 years and IgG lambda MGUS. Re-examination of muscle biopsy revealed amyloid deposition, SAP scan negative for systemic AL amyloid. Treated with velcade and dexamethasone but died from amyloid cardiomyopathy 6/12 later.73 year-old man with painless deltoid weakness. Muscle biopsy revealed plasma cells infiltrate and lightchain deposition with matched lightchain restriction in bone marrow, IgG kappa paraprotein=8 g/L. Cyclosporin and dexamethasone were recommended for infiltrative multifocal, myopathic plasmacytoma.28 year-old female with pain, fatigue and pelvic-girdle weakness was diagnosed with haemophagocytic lymphohistiocytosis without systemic lymphoma or connective tissue disease. Muscle biopsy demonstrated T-cell and macrophage infiltration. Muscle symptoms are responding to steroids, mycophenolate, cyclosporine and etopiside. An allogenic bone marrow transplant is planned.We describe four cases of progressive myopathic weakness as the primary manifestation of an underlying haematological disorder.

Background Observational data suggest intravenous immunoglobulin (IVIg) increases risk of thromboembolic events (TEE). Traditional vascular risk factors influence individual risk but the pro-coagulant mechanism of IVIg is not understood. Aims To ascertain frequency of and risk factors for arterial (ATE) and venous thromboembolic events (VTE) in neuromuscular patients receiving regular IVIg. Methods Diagnosis, dose, frequency, vascular risk factors, pre and post-treatment IgG levels and plasma viscosity were recorded by retrospective casenote review. Results 112 patients received a mean (S.D) dose of 1.6 (1.2)g/kg/month, range:0.2–6.5 g/kg/month; at a mean (S.D.) interval of 4.4 (3.0) weeks, range:1–18 weeks for CIDP (58.9%), MMN (36.6%), sensory neuropathy/neuronopathy (3.7%) and myositis (0.9%). Twelve TEEs were documented during the 30 month study period (January ‘14-June ‘16); 6 MIs, 2 CVAs, and individual occurrences of TIA, DVT, PE, SVC obstruction due to central line thrombosis. TEE incidence (95% C.I.)=53.6 (30.9, 91.3)/1000 patient-years; ATE incidence=35.7 (18.2, 68.9)/1000 patient-years; VTE=22.3 (9.6–51.2)/1000 patient-years. Age (p=0.005) and QRISK2 score (p=0.01) were higher in those who had an event. There was no difference in dose/kg/month (p=0.66), or dose/g/day (p=0.28). Conclusions TEE incidence in this cohort was higher than population-based rates (TEE=7.6–7.7/1000; ATE=4.4–6.5/1000 and VTE=1.2/1000 patient-years). This analysis suggests reduction of daily dose or rate of infusion does little to mediate risk.

To describe the prevalence of distal sensory polyneuropathy (DSP), a complication of both advanced HIV disease and of antiretroviral therapy (ART), amongst Tanzanians with HIV, on and off ART (including stavudine) with CD4 counts above and below 200 cells/μl.We recruited participants attending ART clinic into four groups:6 months ART exposure and (i) CD4200 cells/μl or (ii) CD4200 cells/μl (ART/CD4200 and ART/CD4200, respectively); ART-naïve and (iii) CD4200 cells/μl or iv)CD4200 cells/μl (noART/CD4200 and noART/CD4200, respectively). Primary outcome was DSP, as defined by presence of at least one symptom and one sign.Of 326 evaluable participants, 81 (32 men, median age 38 years, median CD4 142 cells/μl) were enrolled in the ART/CD4200 group, 78 (17 men, median age 37 years, median CD4 345 cells/μl) in ART/CD4200, 81 (30 men, median age 37 years, median CD4 128 cells/μl) in noART/CD4200 and 86 (22 men, median age 33 years, median CD4 446 cells/μl) in noART/CD4200. Numbness was the most commonly reported symptom. DSP prevalence ranged from 43.2% in ART/CD4200 to 20.9% in noART/CD4200. DSP was more common among men (adjusted odds ratio [aOR] 1.9, 95% confidence interval [CI] 1.2-3.3) and older participants (aOR 2.7, 95% CI 1.1-6.2 for age 40 + vs.30 years).Distal sensory polyneuropathy is common amongst those attending this clinic, even those with no ART exposure and a CD4 count above 200 cells/μl. Stavudine and didanosine expose HIV-infected patients to an additional avoidable risk of DSP. Access to non-neurotoxic ART regimes as well as earlier HIV diagnosis and initiation of ART is needed.

The spinal cord and the thoracic and lumbar posterior root ganglia (PRGs) of 14 HIV-positive men and 7 age- and sex-matched controls were studied by routine histology, morphometric analysis of the number of nodules of Nageotte (nN) and the diameters of sensory ganglion cells, immunohistochemistry and in situ hybridization. In 7 patients (2 of whom had evidence of cytomegalovirus ganglionitis) there were increased numbers of nN and diffuse, mild infiltration with CD45R+ T lymphocytes; no B lymphocytes were observed. Macrophages were increased in number in all cases. Whenever more than one ganglion was examined from the same patient, the appearances were similar in all. There was no alteration in the distribution of ganglion cell diameters. Changes in the spinal cord included vacuolar myelopathy (5 cases), HIV myelitis (1 case), microglial nodules (3 cases) and pallor of the gracile tracts (GTP) in 7 cases, in 6 of whom it co-existed with increased numbers of nN. Seven cases had no abnormalities, except the increase in number of macrophages in PRGs. In spite of a correlation between sensory nerve cell loss and GTP our findings suggest that other mechanisms, such as 'dying back' may contribute to the pathogenesis of GTP. Moreover, sensory disturbances were found most commonly in association with nerve cell loss; however, loss of sensory ganglion cells was not necessarily associated with evidence of sensory impairment.

Hereditary angio-oedema is an autosomal dominant condition resulting in a deficiency of C1 esterase inhibitor protein in serum. The condition is characterized by oedematous attacks in the skin, mucous membranes and gastrointestinal tract triggered by mental and physical stress. We present the rare case of a young girl with known hereditary angio-oedema and spina bifida occulta being admitted for an elective pilonidal sinus excision. This case presented different challenges for the anaesthetists and surgeons.

Varicella zoster virus (VZV) is an uncommon but well recognized cause of neurological disease in HIV-infected patients. Analysis of cerebrospinal fluid (CSF) using the polymerase chain reaction (PCR) in HIV-infected patients presenting with neurological disease has increasingly allowed diagnosis of VZV-associated pathology. We report clinical, radiological and virological data from 15 consecutive patients with VZV-associated neurological disease. Clinical presentation was varied, including meningo-encephalitis in 9 and isolated cranial nerve palsies in 6. VZV deoxyribonucleic acid (DNA) was detected by PCR in CSF of 11/15; pleocytosis was present in only 6/15, raised protein in 11/15. Magnetic resonance imaging (MRI) appearances were focal signal abnormalities in 8, meningeal enhancement in 2 and normal in 2. With specific anti-VZV therapy 10 patients recovered fully. The predictive value of PCR on CSF for diagnosis of VZV-associated neurological disease should take into account the patient's clinical presentation, concurrent infections and response to anti-VZV therapy.

CMTX1 is the second most common cause of Charcot-Marie-Tooth disease (CMT), usually caused by mutations in the Cx32 gene. Cx32 has two tissue-specific promoters: P1, specific for liver and pancreas, and P2 which is nerve specific. Over 300 mutations have been described in Cx32 , spread throughout the coding region. However, 10% of CMTX1 families do not have mutations in the coding region. To date, 5 noncoding region mutations have been reported. We describe two families with X-linked inheritance and a phenotype consistent with CMTX1 who did not have mutations in the Cx32 coding region. Family 1 were negative for mutations in PMP22, MPZ, SPTLC1 and GDAP1 Family 2 were negative for mutations in MPZ and rearrangements at chromosome 17p11.2. The noncoding region of Cx32 was sequenced and an upstream exon-splicing variant found at c.-373G>A which segregated with the disease in both families. This variant is located at the last base of the nerve-specific 5′UTR exon and thus may disrupt splicing of the nerve-specific transcript. Online consensus splice-site programs predict a reduced score for the mutant sequence vs the normal sequence. Two other mutations have previously been described within the 5′UTR region, which created a potential donor splice site and were shown to prevent translation of mutant mRNA. It is likely that other mutations within the Cx32 noncoding regions account for the CMTX1 families who do not have coding region mutations.

Twenty four patients who had undergone temporal lobe surgery for epilepsy were assessed to determine (a) whether or not they had developed a visual field defect and (b) if a field defect was present, were the visual field criteria, as required by the DVLA, fulfilled using the monocular Goldmann perimeter test and the automated binocular Esterman method performed on a Humphrey perimeter. A field deficit was found in 13 of 24 (54%) using the Goldmann perimeter and 11 of 24 (46%) by the Esterman method. The second was a more lenient assessment with six of 24 (25%) failing the driving criteria compared with 10 of 24 (42%) by the monocular Goldmann method. Three patients were seizure free but failed the driving criteria. This complication of surgery for temporal lobe epilepsy needs to be discussed with patients before surgery.

It is generally accepted that while inflammatory demyelinating neuropathies often cause patchy demyelination resulting in conduction block, temporal dispersion and variation in conduction velocities, demyelinating hereditary neuropathies such as Charcot–Marie–Tooth (CMT) disease type 1A are usually characterised by homogeneous slow conduction. X-linked CMT is caused by mutations in the gap junction beta 1 ( GJB1 ) gene encoding connexin 32, a gap junction protein, resulting in intermediate conduction velocities. At our institution, mean median nerve conduction velocity in men with GJB1 mutations is 33.2 ± 7.5 m/s (n = 13) and 47.7 ± 7.0 m/s in women (n = 8), similar to other recent series.1 2 There is increasing evidence that nerve conduction is not always homogeneous in GJB1 associated CMT.1–4 Here we present three cases in which the neurophysiology suggested an inflammatory demyelinating neuropathy, but who failed to respond to treatment and were subsequently found to have mutations in GJB1 . ### Case No 1 A 23-year-old man presented with parasthesia affecting both feet that progressed to mild hand parasthesia and weakness over 6 months. Although slightly clumsy, he had been good at sport as a teenager. He had minimal wasting but normal power in his hands, he was areflexic and had reduced vibration and pinprick distally. CSF was acellular, with a raised protein of 0.78 g/l. His initial nerve conduction studies (NCS) (done elsewhere) suggested chronic …

Patients with dystonic syndromes sometimes develop increasingly frequent and relentless episodes of devastating generalized dystonia which we call status dystonicus. Twelve cases of status dystonicus, of various underlying aetiologies, are presented. Possible precipitating factors were identified in only five cases: intercurrent infection (one); discontinuation of lithium (one) and tetrabenazine (one); and the introduction of clonazepam (two). Nine patients required mechanical ventilation and three others were sedated with intravenous chlormethiazole. Drug therapy used included benzhexol, tetrabenazine, pimozide, baclofen, chlorpromazine, haloperidol, carbamazepine and acetozolamide. Two patients underwent thalamotomies, one of whom improved. Two patients died, five returned to their pre-status dystonicus condition, two eventually made a full recovery and three were worse. Patients with status dystonicus should be managed on an intensive care unit as they may develop bulbar and respiratory complications which may require ventilation. Metabolic problems encountered can include rhabdomyolysis with acute renal failure. Drug therapy with benzhexol, tetrabenazine and pimozide or haloperidol may be beneficial in some cases.

HIV distal sensory polyneuropathy (DSP) is the commonest neurological complication of HIV in sub-Saharan Africa. Our data shows between 20.9 and 43.2% of Tanzanians with HIV have DSP depending on risk factor exposure with a similar prevalence reported in other studies. Advanced HIV and a low CD4 count are known risk factors as are nucleoside reverse transcriptase inhibitors (NRTIs) which are present in all anti-retroviral treatment (ART) regimes. HIV DSP is also clinically similar to DSPs caused by nutritional deficiencies, diabetes and alcohol. Accurate diagnosis of HIV DSP is thus problematic, particularly in resource-constrained settings with limited access to investigations. Whilst recent WHO recommendations suggest earlier ART initiation with omission of cheaper neurotoxic NRTIs from formularies, financial constraints often preclude their implementation. A lack of medical infrastructure, particularly at the primary level, makes screening for, monitoring and management of HIV DSP difficult. Existing treatments for HIV DSP neuropathic pain are ineffective and often expensive or unavailable. There is little public health planning relating to HIV DSP in sub Saharan Africa and few data on the scale of disability it causes or its socioeconomic cost. We present a review of recent data relating to HIV DSP in sub Saharan Africa, highlight the challenges this epidemic presents and propose a protocol to screen for and manage HIV DSP in a resource-constrained outpatient setting.

Background Distal sensory polyneuropathy (DSP) is a well-known complication both of advanced HIV disease and of antiretroviral treatments (ARTs), in particular stavudine and didanosone. Both are widely used in sub-Saharan Africa. There are few data documenting the prevalence of HIV DSP in African settings. Aim To describe the prevalence of DSP among Tanzanian patients with HIV, on and off ART and with CD4 counts above and below 200×10 6 /l. We recruited HIV-positive clinic attendees into four groups: >6 months ART exposure and (i) CD4 200 cells/μl; ART naive and (iii) CD4 200 cells/μl. Primary outcome was DSP as defined by presence of at least one symptom and one clinical sign elicited with the ACTG screening tool for DSP. Results 335 subjects were recruited. Nine were excluded. Subject numbers were 81 (ART 200), 81 (noART/ 200). Prevalences of DSP in each group were ((ART/ 200) 41.3% (% CI 30.5 to 53.5)). ((noART/ 200) 20.9% (% CI 12.0 to 29.4)). Conclusion HIV DSP is frequently present even amongst otherwise largely asymptomatic patients. Stavudine and didanosone expose HIV patients to an avoidable risk of DSP with significant morbidity and an impaired quality of life. Diagnosis and management of DSP is inadequate. Access to nonneurotoxic ART regimes as well as earlier diagnosis and initiation of ART is needed.

Arriving at a firm diagnosis of neurosarcoidosis continues to pose serious problems, particularly when evidence of granulomatous disease outside the nervous system is lacking. The commonest mode of presentation of neurosarcoidosis is with cranial nerve palsies. Two cases of presumed neurosarcoidosis with cranial nerve palsies showed clear evidence of focal meningeal disease on gadolinium-DTPA enhanced MRI brain scans. Although not specific for sarcoidosis, this technique may be very useful in aiding the diagnosis in suspected cases.

A patient with small cell carcinoma of the lung developed asymptomatic autonomic neuropathy, inappropriate antidiuretic hormone (ADH) secretion and Lambert Eaton myasthenic syndrome. The autonomic neuropathy and inappropriate ADH secretion were present at the time of diagnosis of the tumour. Following chemotherapy these resolved, but 5 months later the patient developed Lambert Eaton syndrome which responded to 3,4-diaminopyridine. This sequence of changes appears to be unique.

We present a case of Haemophilus influenzae lobar pneumonia in the father of a child admitted with acute epiglottitis caused by the same organism. The suggestion that adult, as well as child, contacts for Haemophilus influenzae epiglottitis should be prophylactically treated is discussed.

Summary A patient with calcific constrictive pericarditis due to rheumatoid arthritis is presented: the literature reveals only one previous case which was attributed to the long duration of the rheumatoid arthritis.

A 33 year old right handed male injection drug user presented with a 4 week history of progressive shoulder and upper arm weakness and difficulty in speaking, together with a 2 week history of fever and a productive cough. He had been HIV-1 antibody positive for 16 years, had no AIDS defining illness, and was on no antiretroviral therapy. The CD4 count was 110 cells ×106/l and viral load was 56 000 copies/ml. There was no past history of, nor had the patient recently been vaccinated against, poliomyelitis; the patient was HB anticore and hepatitis C antibody positive. There was no family history of neurological disease. On examination there were signs of …

Trimethylarsine oxide, a probable intermediate in the biological transformation of arsenate, was reduced to volatile trimethylarsine by Candida humicola. A simple assay for the rate of trimethylarsine production from trimethylarsine oxide by the fungus was developed. The optimum pH for the reduction was determined as 5.1–5.2, and the optimum temperature was 40 °C. The rate of reduction was directly proportional to cell concentration and followed Michaelis–Menten type kinetics. There was almost no trimethylarsine produced by heated or broken cells. The reaction was inhibited by a number of electron transport inhibitors and uncouplers of oxidative phosphorylation including cyanide, azide, and 2,4-dinitrophenol. The rate of reduction was modified by arsenate, methylarsonate, dimethylarsinate, selenate, and tellurate. Preincubation of cells with trimethylarsine oxide increased the rate of reduction 69-fold; this increase in activity was blocked if the cells were incubated with the protein synthesis inhibitor cycloheximide.