Negative symptoms presenting as neuropsychiatric manifestation of vitamin B12 deficiency.

Long lists of psychiatric illness or symptoms have been documented to be caused by vitamin B12 deficiency. We describe an atypical case of a young adult who presented with predominant negative symptoms followed by neurological symptoms consistent with vitamin B12 deficiency. The symptoms showed complete remission after vitamin B12 supplementation. The uniqueness of this case is that vitamin B12 deficiency presented with predominant negative symptoms without other psychotic and manic symptoms, which has not been reported previously.

INTRODUCTION

Psychiatric symptoms attributable to vitamin B12 deficiency have been described for decades. The earlier reports are for the most part in accordance with more recent ones, despite being diagnostically less specific in psychiatric and hematological terms. These symptoms seem to fall into several clinically separate categories: slow cerebration; confusion; memory changes; delirium, with or without hallucinations and/or delusions; depression; acute psychotic states; and (more rarely) reversible manic and schizophreniform states.[1] Apart from these conditions, some cases of dementia, violent behavior and fatigue have also been documented to be caused by vitamin B12 deficiency.[2] There are a few case reports of catatonia, attributed to vitamin B12 deficiency.[3] The psychiatric symptoms can develop long before anemia or spinal cord symptoms.[4-6] The most common neurological manifestations are sensory impairment in the form of paresthesias and decreased vibratory and touch sensations and ataxia.[78] In various studies, the neuropsychiatric abnormalities were present in up to 28% of patients in the absence of any change in the hematocrit values or increase in the red cell mean corpuscular volume (MCV).[78] However, we could not come across a presentation as predominant negative symptoms associated with vitamin B12 deficiency in literature. A case of vitamin B12 deficiency is reported which presented with negative symptoms followed by neurological symptoms.

CASE REPORT

Mr. A, a 27-year-old single male, premorbidlywell adjusted, life-long vegetarian, without significant past or family history of psychiatric illness, presented to our out patient department (OPD) in October 2005 with symptoms of 1 year duration. He started with complaints of forgetfulness for several weeks, followed by social withdrawal, paucity of speech, decreased interest in routine and pleasurable activities and apathy. He stopped going to his work and taking household responsibilities unlike his previous self. His selfcare deteriorated markedly, appetite decreased grossly and he lost 5–7 kg weight in 4–5 months. His duration of sleep also increased. During this entire period, patient or family members denied history of sadness of mood, ideas of worthlessness, hopelessness, guilt, nihilism, catastrophe, suicidal ideation, easy fatiguability; loss of executive functions, agnosia, misrecognition, urinary or fecal incontinence; manic and psychotic symptoms. After detailed assessment, the patient was started on Tab. Olanzapine 5 mg/d. Over the next 3–4 weeks, he perceived minimal improvement, but developed bilateral weakness of lower limbs resulting in limping and walking with support. He was referred to neurology outpatient. Neurological examination revealed bilateral loss of proprioception, vibration, light touch and pain sensation in the lower extremities. There was reduced motor strength and the reflexes were symmetrically diminished in the lower extremities with bilateral positive Babinski sign. Upper extremities were spared. Complete blood counts were essentially normal; however, normochromic anisopoikilocytosis and macrocytes were seen in peripheral blood smear. His nerve conduction studies revealed axonal sensory–motor neuropathy. His serum folate and iron levels were within normal limits. Serum vitamin B12 level was found to be markedly diminished– less than 50 pg/ml (normal: 200–950 pg/ml). Test results for intrinsic factor and parietal cell antibodies were found to be negative in his serum and the patient did not give consent for gastric biopsy. Mr. A was diagnosed with subacute combined degeneration of spinal cord due to vitamin B12 deficiency. He received intramuscular vitamin B12 injections and was referred back to Psychiatry OPD. Olanzapine was stopped and he was continued on intramuscular vitamin B12 injections. His psychological and neurological symptoms improved completely over the next 3–4 months and he is maintaining well for the last 2 years.

DISCUSSION

Negative symptoms of schizophrenia are characterized by restricted affect, diminished emotional range, poverty of speech, curbing of interests, diminished sense of purpose and diminished social drive.[9] The primary negative symptoms usually show poor response to drugs and less long term recovery of functioning.[9] The etiology of this patient's vitamin B12 deficiency was not very clear, but when the patient was seen in his most prominent symptoms (i.e. negative symptoms), anemia and spinal cord symptoms were not prominent. Hence, vitamin B12 deficiency could not be suspected. Several factors in this case suggested an organic cause for this patient's psychiatric symptoms, such as no family or past history of psychiatric illness, well adjusted personality without any history of substance abuse, predominant negative symptoms followed by neurological symptoms. Once the organic nature of his psychiatric illness was realized, the patient was investigated accordingly and was given vitamin B12 supplementation. Within 2–3 months of starting vitamin B12 supplementation, his psychiatric symptoms completely resolved and neurological symptoms improved markedly except minimal weakness in his lower extremities. This again suggests the etiology of negative symptoms is associated with vitamin B12 deficiency. Though there is literature to suggest correlation between low folate levels and negative symptoms of schizophrenia,[10] evidence for association of vitamin B12 or other nutritional deficiency with negative symptoms is lacking. This case suggests that predominant presentation with negative symptoms without other psychopathology can be a manifestation of an underlying vitamin B12 deficiency. Therefore, complete case work up is recommended, including measurement of serum vitamin B12 level, in patients presenting only with predominant negative symptoms.

We can only assume that had psychiatric symptoms been recognized and treated in time as a manifestation of vitamin B12 deficiency, development of neurological symptoms in this case could have possibly been prevented.