SIR: The spectrum of mood disorders attributable to traumatic brain injury (TBI) span almost the entire spectrum of psychiatric disorders.1 Secondary mania and hypomania have been reported in a number of medical conditions. Mania has also been associated with TBI. Diagnosis of mania following brain injury is based on DSM-IV criteria for mood disorder due to TBI with manic features or with mixed features.2 As in case of depressive disorders, a manic episode is thought to be a direct physiological consequence of the TBI.
Predisposing factors for development of mania after TBI include damage to the basal region of right temporal lobe and right orbitofrontal cortex in patients who have family history of bipolar disorder.3 Mood disorders after TBI occur at a greater frequency than in the general population with estimates approaching 25% to 50% for major depression, 15% to 30% for dysthymia and 9% for mania.4 A study that examined patients during the first year after TBI to determine the presence of secondary mania found 9% frequency of secondary mania.5 That ratio was significantly greater than that seen in other brain-injured populations (e.g., patients with stroke). However, studies utilizing established psychiatric diagnostic schemes to study these outcomes after TBI are scarce and no studies have included an assessment of psychiatric disorders.6
Despite common occurrence there are relatively few studies that provide clear assistance about diagnosis and management of symptoms following TBI. In addition, neuroanatomical models for mania after TBI have not been proposed. Therefore, case reports have a significant role in the diagnosis, physiopathology and management of mania after TBI.
A manic syndrome after TBI is described in a 17-year-old female patient who had changes on MRI images of right hemisphere.7 Meanwhile left hemisphere lesion is linked to mania in a case report.8 As a result, it is early to conclude that mania is pathology of right hemisphere. On the other hand, growing evidence from structural neuroimaging studies indicates that mania is associated with anatomical abnormalities of the frontal lobe and that its course was found to be independent of cognitive impairment. 9,10
The patient is a 35-year-old woman who developed a manic episode after TBI. Her family admitted her to the psychiatric clinic for enhanced talkativeness, increased psychomotor activities, and decreased need for sleep for 1 week. She was unable to care for her children and her usual social activities were impaired. She becomes irritable when hindered. She had a history of traumatic hemorrhages and intraparenchymal hematoma following a fall from a truck 23 days ago. She had no history of substance abuse or another medical condition beside the brain injury. There was no history of depressive or manic episode in the past and in her first-degree relatives.
She was admitted to psychiatry clinic after discharging from neurosurgery clinic. In mental status examination, her appearance was in accord with her socio-cultural level. She was reluctant about the interview, and eye contact was not established. Her speech was spontaneous and rapid, and it is sometimes uninterruptible. Speech was understandable but some words were poorly articulated because of high rate of speech. Her mood was anxious, and she became irritable when hindered. There were no perceptional abnormalities and orientation was intact. She was alert and awake throughout the interview but distractibility was outstanding. Abstract thinking, judgment abilities and insight were impaired. Psychomotor activation and decreased need for sleep were observed.
Young Mania Rating Scale (YMRS) and Mini-Mental Status Examination (MMSE) score were found 54 and 24, respectively. Routine laboratory tests including thyroid hormones and thyroid stimulating hormone were within normal limits. Nonenhanced axial computed tomography image following 2 days of head trauma showed parenchymal hematoma in right temporal, contusion areas having bilateral hyperdense hemorrhagic areas in temporoparietal lobes, and hyperdense subdural hemorage in left occipitoparietal convexity also has complex fracture in mastoid region of temporal bone and linear fracture in squamosa region of temporal bone.
We administered haloperidol 10mg/day IM for 2 days but symptoms continued. Therefore, clonezepam infusion was added. Phenytoin sodium 300 mg/day was given for prophylaxis of posttraumatic seizures. Psychomotor activation decreased, sleep was regulated and speech slowed down after 1-week treatment. We switched to oral form and continued for 1 week, and then discharged. One month later, the level of YMRS decreased to 38 points; and MMSE increased to 26 points; thus, haloperidol and clonazepam were discontinued.
T1 weighted axial images (1 month later) showed bilateral hyperintense subacute hematoma in the temporal lobes. There was also atrophy in the temporal lobes and dilatation in the temporal horns of lateral ventricles secondary to atrophy.
The diagnosis (manic episode due to a general medical condition) of the case was established according to DSM-IV criteria.2 The general medical condition is TBI. The following manic criteria were defined: i) A distinct period of abnormally and persistently expansive and irritable mood, lasting more than 1 week. ii) During the period of mood disturbance, the following symptoms have persisted and have been present to a significant degree: Grandiosity, decreased need for sleep (she feels rested after only 4 hours of sleep), more talkative than usual and pressure to keep talking, distractibility, and increase in goal-directed activity. iii) The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning, and in usual social activities and relationships with others, and to necessitate hospitalization to prevent harm to self and others.
The symptoms are due to direct physiological effects of a general medical condition, TBI. Symptoms persist throughout daytime and show no fluctuations over the course of day. Patient had no clouding of consciousness and disturbance of cognition. Consequently we can rule out delirium. As a result this case supports the view that manic episode can follow TBI.
Traumatic brain injury affects the patient through several mechanisms: There are primary and secondary effects of traumatic events.1 Primary effect is produced by contact and inertial forces that occur at the time of injury. Primary effects consist of contusion and diffuse axonal injury. Contact forces may result in laceration to the scalp, skull fractures, intracranial hemorrhages, contusions, and intracerebral hemorrhages. Inertial loading results in diffuse axonal injury and eventually in acute subdural hematoma from the tearing of subdural bridging veins. Secondary effects are produced by pathological processes that are initiated at the moment of injury but span a variable period following the traumatic episode. Secondary effects are hematomas (epidural, subdural, intracerebral), cerebral edema, hydrocephalus, increased intracerebral pressure, infection, neurotoxicity. Intracerebral hemorrhages are often multiple, involving frontal and temporal lobes and basal ganglia and may have a delayed onset.
Structural lesions producing mania usually involve basotemporal, paratalamic structures or inferior medial frontal lobe. They have effects that are specific to their locations and neuronal damage. This case had a history of traumatic subarachnoidal hemorrhages and intraparenchymal hematoma following TBI. Although contrary results are present, there are manic episode cases following TBI in the right hemisphere. A study that examined the patient during the first year after TBI found temporal basal polar lesion as a major correlate of secondary mania.4
Our case has also parenchymal hematoma in right temporal lobe and hyperdense hemorrhagic areas in left temporopariatel lobe. One study found higher frequency of cortical involvement of mainly right orbitofrontal and basotemporal region in the brain of the manic patients.11 These reports are in accordance with our case’s findings. Although this case had no history of a psychiatric illness, a study that examined the rate of psychiatric illness one year after TBI found that a history of psychiatric illness is a risk factor for development of psychiatric illness.12 Also secondary mania was not found to be associated with family history, whereas a major correlate was the presence of a temporal basal lesion.
In addition, there are a number of nonimaging studies suggesting that manic states are associated with greater right than left hemisphere prefrontal and subcortical impairment, and greater ventral than dorsal cortical impairment. Bipolar disorder may be associated with heightened activity in a frontal cortical—subcortical neural system that includes the anterior cingulate and caudate.13 Nonetheless, there are a few consistent findings among these studies. Structural imaging studies suggest an increased number of white matter hyperintensities in patients with bipolar disorder. Decreased cerebellar size and anomalies of cerebellar blood volume have also been reported. Increased sulcal prominence and enlargement of the lateral and third ventricles are less consistently observed findings.14
In conclusion, to our knowledge, no manic cases have been reported after bilateral temporal hemorrhagy. Clinicians must be aware of manic symptoms following bilateral temporal lesions and check the symptoms. More research is needed to definitely elucidate underlying mechanisms of manic symptoms following bilateral temporal hemorrhage.