A woman who was compulsorily hospitalised for manic psychosis proved to need quite different treatment from what was first assumed necessary.
Given her physical restlessness, reduced need for sleep, pressured speech and elated mood calling for hospitalisation, the patient fulfilled the diagnostic criteria for acute mania (Table 1) (1). Because of the acute onset, delirium (acute confusion) was a possible differential diagnosis, but it was regarded as improbable because she was oriented with respect to time, place and situation, and neither the content nor the level of her consciousness was altered. Nor were there any factors that might cause a disposition to delirium, such as fever, metabolic disorder, abuse of drugs/alcohol or dementia. No significance was attached to the pain in her neck and shoulder at this point.
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Table 1 Diagnostic criteria for mania (ICD-10). For a diagnosis to be made, A plus at least 3 B symptoms must be present.
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A.
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Elated, expansive or irritable mood for at least a week or hospitalisation is required
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B.
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At least three of the following symptoms (four if mood is only irritable)
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a.
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Increased activity/physical restlessness
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b.
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More talkative
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c.
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Flight of ideas or subjective sense of racing thoughts
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d.
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Loss of usual social inhibitions resulting in inappropriate behaviour
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e.
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Decreased need for sleep
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f.
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Strongly inflated self-esteem or grandiosity
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g.
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Distractibility or constant changing of plans or activity
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h.
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Risky or reckless behaviour
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i.
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Pronounced increase in sexual energy or uncritical sexual behaviour
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The moderate effect of medication, the patient’s age, pain and neurological symptoms in the form of unsteadiness and impaired walking function led to the suspicion that the patient’s mania was secondary to a neurological disease. Following neurological examination, she was therefore moved to the Neurology Department for further assessment, two days after her arrival.
Neck pain, reduced strength in the right hand and cerebral symptoms in the form of mania accompanied by an elevated cell count in the spinal fluid gave rise to suspicion of a combination of meningoradiculitis and encephalitis, probably caused by a virus or a borrelia infection (neuroborreliosis). Other possible causes, such as purulent bacteria infection or an autoimmune disease/vasculitis were regarded as less probable because of the lack of systemic signs of infection, the mononuclear appearance of the leukocytes and normal blood tests.
The diagnosis of definite neuroborreliosis is based on clinical neurological symptoms accompanied by the findings of an elevated number of leukocytes in the cerebrospinal fluid and a positive borrelia antibody index. The suspicion of neuroborreliosis in our patient was maintained in an early phase and treatment was completed even though the antibody index was negative in the first two cerebrospinal fluid tests. The diagnosis was confirmed after two months, when the antibody index was positive. The antibody response is often delayed in borrelia infections (2). In an early phase of neuroborreliosis (symptom duration less than six weeks) the antibody index is negative in about 26 %, and serum may also be antibody negative. Our patient was almost symptom-free after the antibiotics treatment, but after a while noticed reduced working capacity and tiredness. Recurrence of the infection was suspected, but a normal cell count in the cerebrospinal fluid disproved this. The presence of antibodies alone did not indicate an active infection. It has recently been shown that about 50 % of patients suffer from tiredness 30 months after being treated for neuroborreliosis.
Discussion
Mania is a pathological condition characterised by an elated mood and heightened physical and mental activity. The mood is not in keeping with the patient’s situation, and may vary from carefree joviality to uncontrollable exhilaration. The exhilaration is accompanied by increased energy which leads to overactivity, incessant talking and a reduced need for sleep. Attention cannot be retained, and the person is easily distracted. Self-esteem is often inflated, with grandiosity and excessive self-confidence. Loss of normal social inhibitions may lead to behaviour that is frivolous, reckless or inappropriate and atypical of the person. Mania can be confused with delirium – a state of confusion that is characterised by acute onset, disorientation, visual hallucinations and a fluctuating level of consciousness (4).
Mania is often part of bipolar disorder (primary mania), but there may also be many other causes (secondary mania). The lifetime prevalence of primary mania is 1 % (5). The prevalence of secondary mania is far more difficult to quantify because of great variation in the different sub-groups. Secondary mania may be due to medication, intoxicants, metabolic disturbances or neurological disease (Table 2) (6). It may be difficult to identify secondary mania. Advanced age and somatic symptoms point to increased suspicion. Elderly adults are in the danger zone because of a higher prevalence of medical and neurological diseases. Mania in the elderly is often incorrectly diagnosed as dementia with agitation (7).
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Table 2 Somatic causes of secondary mania (modified from (6))
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Medication
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Intoxicants
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Metabolic disorders
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Neurological disease
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Anabolic steroids
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Alcohol
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Anaemia
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Cerebrovascular disease (particularly right side)
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Antidepressants
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Amphetamine
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Cushing’s syndrome
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Dementia
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Benzodiazepines
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Ecstasy
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Electrolyte disorder
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Encephalitis
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Captopril
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Cocaine
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Hyperthyreosis
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HIV infection
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Enalapril
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Metamphetamine
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Influenza
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Huntingdon’s Disease
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Oestrogen
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Uraemia
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Neurosyphilis
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Calcium
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Vitamin deficiency (B12, niacin)
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Sydenham’s chorea
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Levodopa
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Traumatic brain injury
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Lithium overdose
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Tourette’s disease
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Termination of steroids
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Tumor cerebri
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Steroids
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Wilson’s Disease
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Sympathicomimetics
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It is worth noting that mania and other psychiatric symptoms may be due to neurological disease even if the image representations of the brain (CT, SPECT and MRI), electroencephalography (EEG) and blood tests are normal. This increases the need for a thorough neurological examination, including spinal fluid analysis, in an early phase. Spinal fluid tests may be useful for identifying infection (neuroborreliosis, neurosyphilis, viruses and other infectious agents that may cause encephalitis), carcinomatosis, autoimmune diseases and some neurodegenerative diseases (dementia, Creutzfeldt-Jakob’s Disease) (8).
Lyme borreliosis is a tick-borne infection caused by the spiral bacterium Borrelia burgdoferi. The disease may be localised to the skin (erythema migrans) or disseminated to other organ systems, most commonly the nervous system. Most cases of disseminated disease that are reported to the Norwegian Surveillance System for Communicable Diseases (MSIS) come from the counties of Aust-Agder, Vest-Agder, Vestfold, Telemark, Sogn og Fjordane and Møre og Romsdal, but cases have also been reported further north in Norway (8).
Borrelia infection in the nervous system (neuroborreliosis) may give rise to a number of different symptoms that are all accompanied by an elevated number of mononuclear leukocytes in the cerebrospinal fluid (7). The most common symptoms are pain (located in the neck, back, chest, abdomen or limbs) due to meningoradiculitis, and facial paresis. In rare cases, the infection may attack the central nervous system and cause confusion, tremor and other involuntary movements, unsteadiness, single-side paralysis, aphasia and psychosis. The diagnosis neuroborreliosis is based on the presence of neurological symptoms combined with a concurrent elevated number of lymphocytes in the cerebrospinal fluid and borrelia antibody production revealed by a high ratio between the levels in spinal fluid and serum (also called positive antibody index). However, the antibody index in cerebrospinal fluid is negative in about 26 % of patients in the early phase (symptom duration less than six weeks), and serum may also be antibody negative (9). Fewer than half have a definite elicited history with a tick bite or erythema migrans. Antibiotic treatment results in rapid relief of symptoms and should be started as soon as there is clinical suspicion of neuroborreliosis and a high number of lymphocytes are found in the spinal fluid. The elapse of a long period from the onset of symptoms to treatment is associated with a higher frequency of long-term problems (3, 10). Doxycycline tablets 200 mg daily for 14 days is just as effective as intravenous ceftriaxone in cases of affection of the peripheral nervous system (facial paresis and meningoencephalitis), but for encephalitis many would recommend intravenous ceftriaxone twice daily for 14 days (11).
Our patient suffered from mania caused by borrelia encephalitis. Various psychiatric symptoms of neuroborreliosis have been described (12, 13), but the onset of a manic pathological picture has not previously been described in Europe. A case history from North America describes a patient who developed a bipolar-like syndrome with both depression and mania as the first symptoms of borrelia infection (14). The many manifestations of neuroborreliosis indicate that it should be regarded as a possible differential diagnosis and cerebrospinal fluid should be tested on the first manifestation of psychotic illness, particularly when it is accompanied by pain.
Conclusion
In the case of first-episode psychosis, including mania, a neurological cause should be considered even if the image representation of the brain and the blood tests are normal. Neuroborreliosis and other encephalitic diseases are diagnosed by means of spinal fluid tests, and rapidly applied treatment improves the prognosis.
