Icd 10 major neurocognitive disorder due to traumatic brain injury

Traumatic Brain Injury (TBI) is an intracranial injury that occurs when an external force injures the brain. When clinically significant, the DSM-5 diagnoses are major neurocognitive disorder or mild neurocognitive disorder due to Traumatic Brain Injury.[1]

Epidemiology

About 2% of the population lives with TBI-associated disability. Males account for the majority of TBI cases. The leading causes of TBI are due to falls, motor vehicle accidents, contact sports, and assaults.[2] There are three peak mean ages of highest TBI incidence, including 0–4 years, 15–19 years, and over 65 years.[3]

Prognosis

Neuropsychiatric symptoms tend to be most severe in the first few months following a TBI. In mild-moderate TBI, the typical course is complete or substantial improvement of neuropsychiatric symptoms. Approximately 80% of all TBIs are of mild severity.[4] The symptoms associated with mild TBI resolve within days to weeks after the injury, with complete resolution typical by 3 months. Neuropsychiatric symptoms such as depression, irritability, fatigue, headache, photosensitivity, sleep disturbance also tend to resolve in the weeks following mild TBI.

In moderate to severe TBI, seizures (particularly in the first year), photosensitivity, and hyperacusis can remain. Neuropsychiatric symptoms such as irritability, aggression, depression, sleep disturbance, fatigue, and apathy can occur. These changes can lead to significant psychosocial impairment compared to the pre-injury level, and deterioration in interpersonal relationships. Moderate and severe TBI are associated with increased risk of depression, PTSD, aggression, and possibly neurodegenerative diseases such as Alzheimer's disease.

Older Adults

Those aged >75 years have the highest incidence of TBI of any group.[5] The most common mechanism of injuries are falls from standing height and motor vehicle accidents. In this older cohort, women are affected more than men. There is an increased risk of intracranial bleeding (even in those with mild TBIs).

Older adults generally also have higher morbidity and mortality, slower recovery, and worse functional outcomes.[6] The impairment in cognitive domains post-TBI may improve within the first 6 to 12 months, but keeping an age-related dementia on the differential diagnosis is important. Additionally, the increased frequency of pre-existing and co-morbid medical conditions make TBI outcome assessments challenging, and it can be hard to isolate the effect of the TBI alone. Though age is an important prognostic factor for recovery in TBI, it is not the sole determining factor. Older adults with TBI can have similar outcomes as their younger cohorts.[7]

Comorbidity

Individuals post-TBI have a higher chance of developing depression and posttraumatic stress disorder (PTSD).[8] Although substance use is high before the onset of a TBI, it in fact declines after injury.[9] PTSD can have symptoms such as anxiety, irritability, insomnia, personality changes, and memory problems, and this overlap can sometimes complicate the diagnostic picture.[10]

Criterion A

The criteria are met for major or mild neurocognitive disorder

Criterion B

There is evidence of a traumatic brain injury—that is, an impact to the head or other mechanisms of rapid movement or displacement of the brain within the skull, with one or more of the following:

1. Loss of consciousness.

2. Posttraumatic amnesia.

3. Disorientation and confusion.

4. Neurological signs (e.g. - neuroimaging demonstrating injury; a new onset of seizures; a marked worsening of a preexisting seizure disorder; visual field cuts; anosmia (loss of smell); hemiparesis).

Criterion C

The neurocognitive disorder presents immediately after the occurrence of the traumatic brain injury or immediately after recovery of consciousness and persists past the acute post-injury period.

Concussions can be considered a form of mild traumatic brain injury. A regional study of Canadian adolescents found that approximately 20% of all adolescents have sustained a concussion[11]

Chronic traumatic encephalopathy (CTE) is a term used to describe brain degeneration likely caused by repeated head trauma. CTE is thought to significantly increase the risk for dementia.[12] A diagnosis of CTE can only be made during autopsy. CTE is a rare condition and usually found in individuals who play contact sports.

Symptoms and Severity

Symptoms

The cognitive presentation and symptoms after a TBI can be variable. Difficulties in the domains of complex attention, executive ability, learning, and memory are common as well as slowing in speed of information processing and disturbances in social cognition. In more severe TBIs that involve brain contusion, hemorrhage, or a penetrating injury, there can be more neurocognitive deficits, such as aphasia, neglect, and constructional dyspraxia. TBIs are also associated with:

1. Affective changes (irritability, easy frustration, tension and anxiety, affective lability)

2. Personality changes (disinhibition, apathy, suspiciousness, aggression)

3. Physical changes (headache, fatigue, sleep disorders, vertigo or dizziness, tinnitus, hyperacusis, photosensitivity, anosmia, reduced tolerance to psychotropic medications)

4. Loss of smell can often occur due to sinonasal tract disruption, direct shearing or stretching of olfactory nerve fibers at the cribiform plate, or local contusion or bleeding within the olfactory bulb and cortex.[13]

5. Seizures, hemiparesis, visual disturbances, cranial nerve deficits (particularly in more severe TBI, neurological symptoms and signs)

Severity

Severity ratings for traumatic brain injury

In the First Few Months After a TBI...

It's important to look out for:

Depending on the neuroanatomical region of the injury, symptoms of TBI can vary as described above. In general, TBIs can cause a variety of cytotoxic processes, including axonal injury, free-radical injuries, changes in Mg+2 and Ca+2 signalling, and neurotransmitter excitotoxicity. These changes contribute to a range of cognitive and neuropsychiatric symptoms.

In some instances, the severity of neurocognitive symptoms may appear to be inconsistent with the severity of the TBI. After previously undetected neurological complications (e.g., chronic hematoma) are excluded, the possibility of diagnoses such as somatic symptom disorder or factitious disorder need to be considered. Posttraumatic stress disorder can co-occur with the neurocognitive impairment and have overlapping symptoms (e.g. - difficulty concentrating, depressed mood, aggressive behavioural disinhibition).

Biomarkers for acute concussion have been identified, including ubiquitin carboxy-terminal hydrolase L1 (UCH-L1).[14] The FDA has recently approved this for clinical use.

There are no approved pharmacological treatments for TBI, and use is off-label to address neuropsychiatric symptoms related to the injury.[15] A variety of medications can be used depending on the symptom.

If there is no urgent or acute symptoms, do watchful waiting and assess for spontaneous resolution of symptoms first. A “start low and go slow” approach is important as those with TBI have increased sensitivity to to cognitive side effects of psychotropic and neurological medications.

TBI-related Cognitive Deficits

Depression

Aggression/Agitation

Somnolence

Traumatic Brain Injury (TBI) Guidelines

For Providers

Articles

2) Lauterbach, M. D., Notarangelo, P. L., Nichols, S. J., Lane, K. S., & Koliatsos, V. E. (2015). Diagnostic and treatment challenges in traumatic brain injury patients with severe neuropsychiatric symptoms: Insights into psychiatric practice. Neuropsychiatric disease and treatment, 11, 1601.

3) Lauterbach, M. D., Notarangelo, P. L., Nichols, S. J., Lane, K. S., & Koliatsos, V. E. (2015). Diagnostic and treatment challenges in traumatic brain injury patients with severe neuropsychiatric symptoms: Insights into psychiatric practice. Neuropsychiatric disease and treatment, 11, 1601.

10) Tanev, K. S., Pentel, K. Z., Kredlow, M. A., & Charney, M. E. (2014). PTSD and TBI co-morbidity: scope, clinical presentation and treatment options. Brain injury, 28(3), 261-270.

14) Mondello, S., Palmio, J., Streeter, J., Hayes, R. L., Peltola, J., & Jeromin, A. (2012). Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) is increased in cerebrospinal fluid and plasma of patients after epileptic seizure. BMC neurology, 12(1), 85.

15) Yue, J. K., Burke, J. F., Upadhyayula, P. S., Winkler, E. A., Deng, H., Robinson, C. K., ... & Ngwenya, L. B. (2017). Selective serotonin reuptake inhibitors for treating neurocognitive and neuropsychiatric disorders following traumatic brain injury: an evaluation of current evidence. Brain sciences, 7(8), 93.

16) Silver, J. M., Koumaras, B., Chen, M., Mirski, D., Potkin, S. G., Reyes, P., ... & Gunay, I. (2006). Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology, 67(5), 748-755.

What is major neurocognitive disorder due to traumatic brain injury?

What is the ICD

Is traumatic brain injury a neurocognitive disorder?

What is the ICD