Paraplegia-like symptoms may be a manifestation of organophosphate-induced delayed polyneuropathy. This report details the case of a schizophrenic patient who attempted to commit suicide by ingesting organophosphates, and subsequently exhibited long-lasting paraplegia-like symptoms that were not compatible with objective neurological/ imaging findings. We discuss herein paraplegia-like symptoms that represent a somatic delusion rather than actual neurological symptoms, and which may be a sequela of chronic organophosphate-induced neuropsychiatric disorder (COPIND).
Our patient was a 38-year-old man who had been diagnosed with schizophrenia of a paranoid-type, with onset at the age of 18. At the age of 31, he was found unconscious after drinking an unknown quantity of organophosphates and was admitted to an intensive care unit because of respiratory failure. Two weeks later, the patient complained of bilateral progressive weakness of the lower limbs; however, deep-tendon reflexes and muscle power were preserved, and he denied backache, numbness, radiation of any symptoms to the legs or sphincter disturbance. Nerve conduction velocity (NCV) analysis showed the following: (a) mildly prolonged distal latencies of the sural nerves, (b) mildly generalised delayed F waves, but normal distal latencies and conduction velocities, and (c) a mildly decreased amplitude of the right tibial nerve. Needle electromyography (EMG) was also conducted in order to obtain a complete neuropathic picture, from which it was observed that a number of motor units on the right anterior tibialis remained. The clinical and EMG/NCV findings were therefore not typical of organophosphate-induced delayed polyneuropathy (e.g. no sensory symptoms were present and the ankle jerk reflex was not diminished). Brain computed tomography, electroencephalography (EEG) and magnetic resonance imaging (MRI) were performed, but no cause of paraplegia was identified. On follow-up 2, 4 and 7 years after organophosphate exposure, the patient's clinical presentation remained the same, with similar neurological and imaging study results.
The characteristics of the patient's paraplegia-like symptoms were those of somatic delusion; in this case it consisted of a false belief concerning bilateral motor dysfunction of the lower limbs. The patient had not experienced any thoughts in the form of somatic delusion prior to the ingestion of organophosphates, but developed major symptoms subsequent to exposure, which continued ever since. We believe these to be delusional symptoms; otherwise, they persisted after organophosphate ingestion and proved unresponsive to any of the treatments used.
Paraplegia-like symptoms after organophosphate exposure are a chronic psychotic feature rather than a neurological sign. In addition to his paraplegia-like symptoms, our patient reported a depressed mood and performed poorly in intelligence tests, both of which are symptoms of COPIND. He was therefore administered higher doses of antipsychotic medication following organophosphate ingestion, and a combination of 400 mg clozapine and 9 mg paliperidone daily proved necessary for the treatment of psychosis.
The symptoms of COPIND include cognitive deficit, mood symptoms, psychotic symptoms and autonomic dysfunction, which usually persist for a long while after ingestion, and the occurrence of which is delayed (Reference Metcalf and Holmes1,Reference Savage, Keefe, Mounce, Heaton, Lewis and Burcar2). Cognitive deficit is the main symptom of this disorder, and is similar to the symptoms of cholinergic deficit (Reference Tan, Peng, Wu, Wang, Lu and Yan3).
The following points are noteworthy. First, cholinergic deficit has been showed to cause positive symptoms of schizophrenia, such as hallucination and delusion, in a normal population (Reference Tandon and Greden4), as the cholinergic system modulates dopamine release (Reference Scarr and Dean5). Second, a chronic consequence of organophosphate ingestion is the functional alteration of multiple neurotransmitter systems within the central nervous system (CNS), such as depletion of serotonin in humans (Reference Ali, Hasan and Tariq6). Serotonergic systems interact with other monoaminergic and glutamatergic systems and contribute to psychosis (Reference Geyer and Vollenweider7). Third, organophosphates have been shown to influence neurotransmitter synthesis, storage and receptors of acetylcholine, serotonin, norepinephrine and dopamine in rats (Reference Slotkin and Seidler8). There is evidence in support of the hypothesis that muscarinic receptors (particularly, muscarinic M1 and M4 receptors) play a role in the pathophysiology of schizophrenia, both in the general population (Reference Scarr9) and in patients who have sustained injury to the brain (Reference Bennouna, Greene and Defranoux10); thus, COPIND might exacerbate psychotic symptoms in patients with schizophrenia by affecting neurotransmitter systems.
Our patient exhibited paraplegia-like symptoms that were not found to be a result of neurological impairment. Thus, we hypothesised that these paraplegia-like symptoms were a type of somatic delusion and a chronic consequence of organophosphate ingestion. Somatic delusion might be a direct consequence of the ingestion of organophosphates and/or may be a result of subsequent exacerbation of an underlying mental illness.
As cholinergic deficit has been shown to cause positive symptoms of schizophrenia in a normal population (Reference Tandon and Greden4), schizophrenic patients may suffer from even more severe and frequent psychotic episodes after exposure to organophosphates. Exposure to organophosphates exacerbated the psychotic symptoms of our patient, and he developed a persistent and treatment-resistant somatic delusion. This shows that the prognosis of chronic schizophrenia patients is worsened by exposure to organophosphates.
COPIND may exacerbate the psychotic symptoms of schizophrenia owing to cholinergic deficit and depletion of serotonin, and organophosphate exposure might therefore result in poor prognosis in patients with chronic schizophrenia.
