Major Depressive Disorder

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Desvenlafaxine depression and neuropathic painBupropion patient with depression, fearful of weight gain and sexual disturbancesBuspirone generalixed anxiety

Traumatic brain injury

Early stage of a moderate to severe TBI encephalopathic states (lasts days to months) ?? Sub-acute TBI patients regain consciousness commonly agitated

and delirous. May require the usage of benzodiazepines in agitated patients Some experts believe that in the very acute stages of TBI, antipsychotics,

esp. atypical antipsychotics, should be avoided since D2 blockade can trigger cell deaths through glutamate cascades furthering the TBI damage.

Intermediate stage if brain injury acute manifestations of the injury are quieting down as the brain enters

the next stage of recovery. Delirium/disorientation is resolving and patients progress toward more

chronic neuropsychiatric syndrome (eg. Behavioral/ personality disturbances, affective dysregulation, and cognitive distortions/paranoia).

During this period, patients typically enter rehabilitation facilities

Late or chronic effects of TBI 6 months to one year after acute injury Emerge as “stable deficits” Syndrome seen dependent upon the area of brain that was damaged, the

extent of damage, and the age of the patient. Frontal lobe damage impairment in memory, executive functioning and

may present with problem in self-regulation. Temporal lobe damage mania and psychosis (temporal lobe epilepsy

syndrome), or affective symptoms and psychosis without associated seizures

Note: for some patients, TBI (as either contributing factors or as the sole cause

of symptoms) is recognized the 1st time in psychiatric inpatient unit! Patient with mild TBI who does not fully recover, may have vague

symptoms headaches, dizziness, sleep disturbance and cognitive impairment as well as anxiety and mood disturbance. often not recognized.

Mild TBI + pre-injury primary psychiatry disorder = more frequent admission and longer stays on the inpatient unit

Patient with TBI may develop subthreshold PTSD symptoms or even frank PTSD especially in patient with history of abuse.

What happens to the brain?o Neuroanatomical and neurochemical disruptionso Primary and secondary injuryo Types of primary injury: Penetrative injuries, compression injuries,

shearing force traumao Coup-countrecoup refer to torsional injury when the head is in motion

where the opposite sides of the brain can be injured at the same time.o Secondary injury: brain edema, hypoxia secondary to cerebral perfusion

pressure, neuronal damage and cytochemical disruption caused by release of excitatory neurotransmitters from injured neurons.

Severity of TBI GCS ( mild 13-15, moderate 9-12, severe 8 or less) Duration of loss consciousness (mild <20 mins, moderate 20-60 mins,

severe >60 mins) Extent of post-traumatic amnesia (> 2 weeks of amnesia severe TBI) Predictive value regarding the likelihood pyychiatric sequale:

All open head injuries Closed head injuries with one or more of the following:

o 15 mins or more of unconsciousnesso skull fracture or intracranial hemorrhageo focal neurological signs at the time of the injuryo seizure at the time of injuryo noticeable period of anterograde amnesia following injury

o prolonged poor functioning post-injury

Pre-morbid factors influencing TBI patient presentation and prognosiso coping mechanismo personality traitso pre-morbid psychiatric vulnerabilitieso severity or extent of injuryo substance use disordero Patient’s psychosocial situation

Note: TBI is a risk factor for another TBI. It is not uncommon for TBI patients to lose support by alienating others with provocative behavioursElements for evaluating inpatient with TBI

o History of the accident: type of accident, period of loss of consciousness, any report of scales used in the acute phase, history of subdural hematoma, surgeries, seizures etc

o Imaging studies and laboratory test (eg.thyroid functions, VDRL, ANA, B12, toxicology, urine drug screen)

o Past psychiatric history (TBI can exacerbates pre-existing illness)o Alloanamnesis may be necessary in case of injury –related amnesia or

current lack of insighto Family psychiatric history (may reveal unexpressed genotype)o Mental status examinationo Others: premorbid functioning, presence of axis II disorders or traits, and

pre-morbid substance useNote: important to note that these patients may be already heavily medicated with opiates and psychotropic, thus extra cautions should be exercised when prescribing additional drugs to prevent drug interactions.

TBI-related syndromeso Mood disorder (depression occur in up to 50% patients)o Pathophysiology neuroanatomy, biopsychosocial perspective with

multi-factorial contributions.o TBI-related depression has a significant suicide rate (15 to 20%)o Post-TBI mania occur less commonly (<10% of cases) either as pre-TBI

bipolar disorder or arising de novo from the injury.o Most common post-TBI psychotic states are paranoid in nature (ranges

from queroluos and suspicious to frankly delusional).o Anxiety states may resemble GAD or panic disorder.o May also take the form of PTSD-like states o Aggressive states and irritability are common sequale of TBI and often

the cause of hospital admission (thought to be related to damage in regions of the orbitofrontal cortex, anterior temporal lobe , amygdala and connecting circuits between those areas).

o In frontal lobe damage flatness of mood, lack of social graces and empathy, and decreased attention to self-care.

Note: Malingering or exaggeration of TBI-related complains are not common. Health care workers often have difficulty accepting that a mild TBI can be associated with more severe lasting neuropsychiatric impairment. Research has shown that the initial severity of illness is not necessarily correlated with the severity of a subsequent post-TBI neuropsychiatric syndrome.

Note:o Family members may become frustrated when the physical aspects of TBI

is improving but emotional symptoms are still persistent require more than usual amount of social work attention.

o Patient with self-loathing may benefit from inpatient groups and activities directed at allowing mouring the lost “pre-TBI self” while building new coping skills.

o Staff’s familiarity and skill at behavioral intervention is necessary effective adjuncts to pharmacotherapy (see table 6.1).

Medication for TBI-related psychiatric symptomso Currently no medications have been FDA-approved for TBI, “off-label use”o Several medications that has been used for TBI includes:

o Medications for TBI should start with low doses and increase slowly (injured brain is more sensitive to the effects of medications)

o Aggression /disinhibiton propranolol, amantadine, antipsychotics, mood stablizers, lithium.

o Clozapine is last resort for TBI-related aggression or psychosis due to increased risk of seizures in patient with TBI

o Difficulties in initiation and attention Stimulants and atomoxetine are most helpful, may also decrease angry outbursts in some patients

o TBI-related depression SSRI or SNRI are helpful, either alone or with combination with mood stabilizer. SSRI/SNRI may cause agitation and over-activation, as well as dystonia, in patients with TBI.

o Sleep disturbance Trazadone and mirtazapine o ECT is indicated for psychotic depression in TBIo Anxiety antidepressant (SSRI, SNRI, TCA or mirtazapine) +/- mood

stabilizer. Benzodiazepine may be used in the early stages of tx but transition to antidepressant should be attempted.

o Combination of tx is common due to the complexity of TBI neuropsychiatric presentatios and the frequency of a multi-symptom picture.

o Psychosocial factors such as interaction with staff and other patients and possible stress from family visits should be assessed whenever patients fail extensive trial of medications.

Patient with both TBI and substance use disordero Getting the patient off the drugs or alcohol in order to treat TBI-related

psychiatric syndromeso Aggresively treating symptoms that may foster substance use disordero Motivational interviewing techniques should be adjusted to deal with TBI

patient cognitive limitations.o Best approach: educational + modified motivational elements (involves

both patient and famly) + attitude from the tx team of “flexibility without indulgence”