Introduction
A case of clinically presumed botulism associated with subcutaneous drug use, in which, the potential utility of the compound muscle action potential responses elicited by the electrical tendon hammer stimulation is presented.

Case
A patient of 47 years presented with 3 weeks of progressive bulbar weakness. He had constipation, general malaise, dry mouth, double vision and swallowing difficulties. He was a known subcutaneous drug user (“popping”) treated with methadone. At the Royal Victoria Infirmary Newcastle neurology unit, observations showed bilateral forearm necrotic tissue, asymmetric ptosis, facial weakness and a complex opthalmoplegia. Deep tendon reflexes were absent. Post-exercise facilitation of the reflexes was not seen clinically. He was treated with amoxicillin and metronidazole, dead tissue related to the subcutaneous drug use was debrided, and botulinum antitoxin administered.

NCS findings at presentation
Nerve conduction studies (NCS) performed at initial presentation showed borderline small compound muscle action potentials (CMAP) (pre-exercise APB CMAP 7mV) and post-exercise facilitation of the CMAP (APB CMAP 14.6mV).
CMAP facilitation following exercise was also seen from percussive stimulation of the biceps deep tendons. The CMAP elicited from deep tendon stimulation decayed over a time interval of approximately 1-2 minutes. This differs from non-Botulism cases.

Follow up
During the acute admission of 17 days, the ptosis, facial weakness and opthalmoplegia resolved. At out-patient follow-up at four months, the constipation and symptoms of the dry mouth had also resolved.  At 1 year follow up these presenting features remained absent.
Subsequently acetylcholine receptor antibody and voltage gated calcium channel antibodies were negative. However, blood tests and the debrided tissue did not demonstrate botulinum toxin using PCR methods
Repeated NCS performed at four months demonstrated resolution of the small CMAPs (APB-CMAP at rest 14.6mV).

Conclusion
Although the diagnosis of botulism is presumed, risk factors, clinical features and a treatment response to a specific treatment for botulism were appropriate to this diagnosis. The NCS showed features of a pre-synaptic neuromuscular junction disorder further supported the diagnosis. Investigations for myasthenia gravis and Lambert Eaton myasthenic syndrome were negative.

Novelty to clinical neurophysiology practice.
Facilitation of the reflexes in presynaptic neuromuscular junction disorders is well known. The novel aspect in this case was the use of the CMAP elicited by the electrical tendon hammer. This had shown post-exercise facilitation reflecting the known facilitation of reflexes that can be clinically seen, though not evident in this case.
Patient consent was obtained for presentation.