Delirium Due to Viral Encephalitis: A Case Report

Delirium Due to Viral Encephalitis: A Case Report

Dr Nihan OĞUZ*, Cem İLNEM **, Ferhan YENER *

Dusunen Adam The Journal of Psychiatry and Neurological Sciences;2005, 18(4):217-223

ABSTRACT

The sign and Symptoms of viral encephalitis vary. Some of these are meningial irritation, headache, nausea and vomiting, fever, changes in consciousness, focal neurological signs, seizures, behavioral changes and delirium. When the primary sign and symptoms are delirium and behavioral changes, the illness could easily be misdiag- nosed. Below, the case presentation of delirium due to viral encephalitis which is treated within 15 days of symp- tom presentation, is described.

Key words: Viral encephalitis, delirium, behavioral changes

INTRODUCTION

Encephalitis is a type of inflammation of the brain. Its etiology in this case is often called viral encephalitis, which is caused by viruses. Different viruses can infect the brain. Among these, herpes and mumps viruses are the leading ones. Some viruses (e.g. measles, chickenpox, rubella) can cause inflammation by the immune system without infecting the brain. Such infections are often referred to as parainfectious encephalitis or postinfectious encephalitis. The inflammation usually develops 5-10 days after getting a viral illness. In rare cases, inflammation can develop weeks, months, or years after a viral infection (1).

Delirium is characterized by impaired consciousness and a cognitive change that develops over a short period of time. The main characteristic of delirium is a disorder of consciousness that is accompanied by a cognitive change that cannot be better explained by pre-existing or entrenched dementia. This disorder develops in a short time, usually within hours or days, and fluctuates throughout the day in data from medical history, physical exam, or laboratory findings. Delirium; There is evidence that general health, substance poisoning or withdrawal, drug use, exposure to toxins, or a combination of these factors are directly related to physiological effects (1,2).

A patient hospitalized for delirium for viral encephalitis is presented below in the light of the relevant literature.

FACTS

Ms. Y, 26 years old, born in Diyarbakır, single, elementary school graduate, lives with her family in Istanbul and applied to our hospital because of seizures and behavioural changes. The patient's relatives learned that her symptoms began 15 days ago with symptoms of nausea and vomiting. No pathological findings were found in the examinations and routine examinations carried out in the inpatient outpatient department, during which symptoms of nausea and vomiting occurred. However, the next day she had seizures (complex partial seizures) in the style of searching for something, accompanied by panic and intense fear, with her eyes deviating to the right. On the same day, the patient developed a headache, nausea, and vomiting, and heard ringing in her right ear. The cranial CT requested by the hospital neurologist turned out to be normal, the EEG was taken, but the patient was referred to the psychiatric ward as no neuropathological findings were found. After this date, these seizures repeated several times, she began to look for something with her eyes deviated to the right, accompanied by panic and intense fear. Citalopram 20 mg/ day was recommended to her by the hospital psychiatrist. The patient took citalopram for two days. On the second day of drug treatment, she had an unlawful secondary generalized tonic clonic seizure with her eyes deviating to the right, turning purple in colour, urinary incontinence, and turning her head and body to the right. This attack lasted about 5-6 minutes. The attack was repeated three times with an interval of 15 minutes. It was stated that the patient who had applied to the psychiatric department of our hospital with these complaints and her family should continue her medication and that she should return to the outpatient department after 3 days.During this time, the patient's seizures stopped, but symptoms such as pulling up the right corner of the mouth, tingling in the right arm, constant sleep, meaningless speaking, and repeating what was said were added. The patient returned to psychiatric control with complaints of "forgetfulness, self-talk, voices in the ear, walking around the house, and skepticism" was observed to be agitated, speak loudly, increase psychomotor activity, and he "bipolar mood disorder with psychotic traits to the manic episode ". She was admitted to the hospital 15 days after the onset of the symptoms with a pre-diagnosis of "psychotic features". Prior to hospitalization, Haloperidol 10 mg Amp IM and Biperiden 5 mg Amp IM were given to sedate the patient. On the ward, when the files showed that her eyes were deviating to the right, her color was purple, accompanied by urinary incontinence, and her head and body turned to the right, resulting in an adverse secondary generalized tonic-clonic seizure recognized. Due to the requested neurological consultation, she was admitted to the neurological intensive care unit for examination and treatment 1 day after the hospital stay. No important characteristic was found in the personality development or in the history of the sick. When investigating any psychiatric or other illnesses in her family, it was found that only her uncle's son had epilepsy. The patient did not use any psychoactive substances, including smoking. There were no characteristics in her psychiatric or medical history.

On her psychiatric examination: her consciousness is slightly drowsy, her psychomotor activity is normal, her mood is cloudy, her orientation to place and time is insufficient, her orientation to the person is complete, the recognition in memory is 4/4, her explanation ¼, her recent history is insufficient, her distant past sufficient. Her attention and focus are reduced, reaction time is increased and the amount of speech is reduced, her associations are slow and smooth, the purpose is on the thought, there is no deception. She was found to have perceived ego dystonic auditory hallucination, paresthesia of "I hear humming noises" and "I have a progressive burning sensation in my leg". She was able to perform simple mathematical operations, had sufficient judgment, abstraction and informational content about current events, and she had insight into her illness. With these results, the decision was made to continue treatment with Chlorpromazine 100 mg tb, Haloperidol 10 mg IM 2X1, Biperiden 5 mg IM 2X1, but neurological counseling was requested immediately.

During the neurological examination in the neurological intensive care unit where she was hospitalized as a result of the consultation, her consciousness is susceptible to sleep due to treatment with diazepam 10 mg 1x1/ 2 IM, which was performed to stop seizures in a neurological emergency . The patient's blood pressure was 130/80 mmHg, pulse was 70 / minute, and body temperature was 36.4 ° C. She was found to be right-handed. There was no evidence of meningeal irritation. Her orientation to place and person was complete, but her orientation to time was distorted. She was reluctant and negative about the investigation. The skull area, muscle strength, and reflex examination were normal. The basal skin reflex was found to be bilateral plantar and extrapyramidal systems, and examination of the cerebellum was normal. In the sensory examination there was no sensory defect apart from the paresthesia described in the left band. Her balance and gait were normal.

In the laboratory test, leukocytes: 10.6 K / ul, neutrophils: 7.49, monocytes: 0.914, SGOT: 75 IU / l (5-50), LDH: 224 IU / l (70-200), CK: 1620 mg / dl (15-240), thyroid function tests, urinalysis, sedimentation, PT / PTT / INR were within normal limits. AntiHBs: 167 mIU / ml, AntiHBc: positive.

At the lumbar puncture, the CSF was clear, there were no cells on microscopic examination, and the glucose and protein levels were within normal limits. Antibodies to herpes simplex virus type I-II and mycoplasma pneumonia were not found in the CSF polymerase chain reaction study. The EEG examination (performed in the first hospital) revealed diffuse disorganization in both frontotemporal regions. 5 days after the first EEG, a bioelectrical disturbance in both hemispheres was found in the right area and neuronal hyperexcitability in the right time. In the EEG 4 days later, bioelectrical disorganization in both hemispheres and the presence of slow-wave paroxysmal activities in both hemispheres were found. In the EEG, which was re-recorded 10 days later, bioelectrical disorganization and intermittent rhythmic delta activities were found in both hemispheres. The cranial MR scan was normal.

At the clinical follow-up, she was observed to have a pulling at the right corner of her mouth, clonic contractions in her right arm, and subfebrile fever. Carbamazepine 100 mg / day, acyclovir 250 mg 2 + 2 + 3 (IV), diazepam amp. 10 mg 1 × 1/2 was started. Carbamazepine was increased to 400 mg and diazepam to 10 mg as the pulling on the right corner of her mouth and clonic contractions in her right arm continued. On the 5th day in the intensive care unit it was observed that the retractions of the right edge of the mouth were still ongoing. Verbal communication became more active. The patient stated that she heard the buzz of flies, human whispers and music noises in her ears as if the piano was being played, but that only she could hear these noises and that these noises would not be possible in the intensive care unit. The next day, the patient said that the noises in her left ear became more intense, she heard the buzz of a fly, the voice of a woman singing, and a ticking sound. She stated that she felt that "there was a child on her chest crying" and that she could stop these noises by coughing. She stated that she had a burning sensation in her left leg and that she felt that her foot was in the water, but she didn't notice any difference when she touched both legs with her hands. She stated that the voices she heard decreased over the next two days, but the sensations in her leg continued. The carbamazepine blood level was 6.91 (4-10) IU / l. Barbexaclon 100 mg / day was added to the treatment as the indentation mark persisted on the right edge of the mouth.

DISCUSSION

Viral encephalitis is an acute febrile illness that causes changes in consciousness, focal neurological findings, and seizures, and damages the parenchymal tissue of the central nervous system (CNS). Although the ethology cannot be established in two thirds of the cases, the use of the polymerase chain reaction technique gradually increases the detection of viral and other agents responsible for the etiology. Viruses transmitted by arthropods (arboviruses), herpes viruses and enteroviruses form the largest category among the detectable pathogens of viral encephalitis. Sporadic cases are mostly caused by the herpes simplex virus. Other less common viruses can be listed as mumps, influenza, herpes zoster, coxsackie, cytomega-lovirus, rubella, rubeola, rabies, enteroviruses, and Epstein-Barr virus (4). The pathogenicity of each virus is different, while some can cause transient neurological dysfunction, some can cause widespread neuronal death. In acute viral encephalitis, damage and inflammation occur in gray matter neurons in the CNS. Neural inclusion bodies are formed in some types of encephalitis, such as rabies and herpes simplex encephalitis; There is a perivascular invasion of lymphocytes and plasma cells and inflammation of the leptomeninges. Certain viruses have affinities for certain regions of the CNS. There are two types of herpes simplex virus (HSV). HSV-I and HSV-II. HSV-I is responsible for the majority of herpes encephalitis. HSV-I encephalitis is an acute, often fatal, necrotizing encephalitis with affinity to the temporal and orbitofrontal regions of the brain. HSV-I is a large, enveloped DNA virus that reaches the brain from the trigeminal ganglion or other regions where it is in the latent state. The virus shows tropism towards neurons in the temporal region of the brain. In these regions, necrosis, areas of bleeding, diffuse mononuclear infiltration, loss of neuronal cells, and intranuclear inclusions in the surviving neurons are noted. There is pronounced brain edema, usually affecting a single temporal lobe or hemisphere, causing asymmetrical swelling of the brain.

Signs and symptoms of viral encephalitis vary depending on the etiological pathogen. Meningeal irritation, headache, nausea, vomiting, fever, photophobia, changes in consciousness, focal neurological findings, and seizures may be present. Seizures are the most common permanent abnormalities. Personality changes, extrapyramidal signs, dementia, and motor sensory disorders can complicate most viral encephalitis.

Herpes encephalitis occurs mainly in children, adolescents, and young adults. In general, a prodromal period, which can last a few days, can be observed with symptoms such as headache, nausea, mild fever, irritability, and fatigue. Its onset can be insidious (weeks, months) or sudden (hours). Typically, it can start with a fever, headache, and delirium. Changes in behavior, partial or generalized seizures, nausea, vomiting, disorientation, and memory disorders are common. Sometimes it can be seen with a psychosis picture made up of strange behaviors and delusions. Focal symptoms, aphasia, and hemiparesis can be observed in patients with advanced hemiparesis (3,5). In our patient Y, the symptoms seem to have progressed within a few days. As with viral encephalitis, symptoms began with nausea, and after 15 days complex partial seizures and panic-like intense anxiety began. In particular, panic-like intense anxiety suggests that the temporal cortex and amygdala may be affected by a viral infection.Ms. Y's fragmentary, unsystematic auditory hallucinations, amnesia affecting near memory, decreased amount of speech, impaired consciousness (prone to sleep), decreased ability to properly maintain attention and move into new areas, impairment (twofold). The fact that it starts within days and fluctuates during the day and all of these symptoms developed within a week suggest a diagnosis of "delirium due to viral encephalitis".Delirium cannot be better explained by pre-existing or developing dementia. It is a disorder of consciousness that is accompanied by a cognitive change.This disorder usually develops over a short period of time, within hours or days, and fluctuates throughout the day. In delirium, psychotic symptoms fluctuate, are fragmentary and unsystematic, occur at a time when the ability to adequately maintain attention or shift attention to new areas decreases, and this is usually associated with EEG abnormalities (general slowdown or fast activity) (2).

Similar findings were found in Ms. Y.

In the etiology of delirium: intoxication (drugs, alcohol, illegal drugs, inhalants, industrial poisons, poisons from animals, plants and fungi), withdrawal syndromes (alcohol, sedatives and hypnotics, amphetamines), metabolic encephalopathies, infections (bacterial meningitis, viral encephalitis, Fungal and protozoal infections, trichinosis, neurosyphilis, post-infectious and post-imitative encephalomyelitis, systemic infections), head trauma, epilepsy, neoplasm, vascular diseases, intracranial extensive lesions, haematopoietic system disorders, hypersensitivity disorders, accidents with physical substances.

Asymmetrical bilateral HSV-I encephalitis affects the hippocampus, amygdala, parahippocampal gyrus, posterior orbital cortex, inferomedial temporal and frontal lobes, which can lead to cognitive loss, especially in the case of memory deficit. The patient's consciousness tended to sleep for days and his complex partial seizures, which began on day 17, turned into unlawful generalized tonic-clonic seizures on day 20. From here we can say that Ms. Y's clinic made rapid progress after the prodromal period.

In the laboratory examination of viral encephalitis, the appearance of the CSF is clear, the pressure is increased or normal. In some cases, there may be an increase in polymorphonuclear leukocytes in the early phase and lymphocytic pleocytosis in the subsequent phase. The amount of glucose is normal. Slightly increased protein.

Our patient's CSF view was also clear, no cells were detected on microscopic examination. The amount of CSF protein and glucose was within normal limits. In viral encephalitis, one or both medial parts of the temporal lobe may be radiolucent on cranial CT. In the cranial MRI, T2-weighted sections (3,5) show an increase in the signal in the medial temporal lobes. The cranial CT and MRI of our patient were evaluated within normal limits. In the EEG examination of viral encephalitis, bilateral, widespread slowdown and a temporal slowdown with periodic sharp waves can be observed in herpes encephalitis (4,5). Similarly, in our patient's EEG, the undeveloped, frequent sharp slow waves in the right temporal domain, then the bioelectrical disorganization in both hemispheres, and the paroxysmal activities of slow waves in both hemispheres were observed. SPECT exams can show a significant increase in perfusion, especially in the temporal lobes. Brain biopsy is a method of definitive diagnosis of viral encephalitis. However, based on the reliable results of the polymerase chain reaction (PCR), brain biopsy has been questioned. An increase in antiviral complement-fixing antibody titers can be observed (3). The antibodies against HSV-I, II and Mycoplasma pneumonia were not found in Ms. Y's CSF polymerase chain reaction.

In differential diagnosis: brain abscess, fungal or bacterial meningitis, toxoplasmosis, other viral Nuchalitis, septic embolization, post-infectious encephalitis, acute necrotizing hemorrhagic encephalitis, Mycoplasma pneumonia encephalitis, Paraneop rubber limbic encephalitis, toxic encephalitis, chlamydia encephalitis syndrome similar attacks should be considered (5,7,8,9,10). The onset and development of our patient's clinical symptoms, the appearance and analysis of the CSF, the EEG findings, as well as her awareness and verbal communication 3 days after the onset of empirical viral encephalitis suggests the diagnosis of viral encephalitis.

Clinical experience: If viral encephalitis is not treated, the death rate is high (20-50%). Herpes encephalitis mortality is 70%. In survivors, Korsakoff's syndrome, KluverBucy syndrome, dementia, aphasia, and hemiparesis can be seen as sequelae (3,5,11,12) of limbic encephalitis. In such cases, it is generally believed that low-dose serotonergic agents are effective in controlling emotional lability (13).
In the treatment of viral encephalitis, acyclovir is the empirical drug of choice that can be used systemically. Medication should be started as soon as possible before the onset of the coma. Brain edema with dexamethasone; Seizures can be treated with anticonvusants such as phenytoin and carbamazepine (3,5,11). In the treatment of acute encephalitis, attention should be paid to the neurotoxicity of acyclovir. Confusion, excitement, and insomnia; Symptoms that can occur with neurotoxicity (14). In addition to acyclovir, vidarabine can also be used for treatment (15).

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