Comorbidities and

Complications of TBI

Rocco A Chiappini, MD

TBI: A Disease Process, Not

an Event

• WHO definition of a chronic disease

– Permanent

– Caused by non-reversible pathological

alterations

– Requires special training of patient

– May require a long period of observation,

supervision or care

Masel and DeWitt,

J Neurotrauma 2010 • TBI increases long term mortality and

decreases life expectancy. It is associated with increased incidence of seizures, sleep disorders, neurodegenerative disease, neuroendocrine dysregulation and psychiatric diseases as well as non-neurologic disorders such as sexual dysfunction, bladder and bowel…

Masel and Dewitt

J Neurotrauma 2010

• … incontinence and systemic metabolic

dysregulation that may arise and/or

persist for months or years after injury.

TBI Complications and

Comorbidities

• Seizures

• Sleep disturbance

• Fatigue

• Infections

• Craniectomy

• Hydrocephalus

• Shunt issues

TBI Complications and

Comorbidities

• Subdural/Epidural Hematoma

• Neuro-endocrine dysfunction

• Spasticity

• Post-traumatic headache

Seizures

• TBI is the leading cause of epilepsy in

young adults

• Early seizures- within the first week

• Late seizures- after the first week

• Incidence of late seizures

– Nonpenetrating severe TBI 17%

– Penetrating TBI 35-65%

Seizures- risk factors

• Depressed skull

fracture

• Bone/metal

fragments

• Focal contusions

• Intracranial

hemorrhage

Gunshot wound

Types of Seizures

• Partial 25%

• Generalized 25%

• Partial with secondary generalization

50%

Frontal Lobe Epilepsy

• Complex, semipurposeful motor

automatisms

Temporal Lobe Epilepsy

• May have emotional symptoms like

panic followed by post-ictal confusion or

amnesia

Seizures

Current Recommendations

• Prophylaxis for the first week

• Discontinue prophylaxis and monitor

• Treat late seizures with carbamazepine,

valproate, lamotrigine or levetiracetam

• Avoid phenytoin

Sleep Disorders

• Guilleminault studied 184 TBI survivors

– Restless sleep 49%

– Regular loud snoring 36%

– Leg and body jerking during sleep 18%

Sleep Disorders

• Ouellet studied 452 TBI survivors (avg

time since injury 8 years)

– 50% had symptoms of insomnia

– 30% met criteria for insomnia (general

public 10%)

Sleep disorders

• TBI population

– Decreased REM

– Decreased total sleep time

– More frequent awakenings

– Decreased deep sleep stages

Sleep Disorders

Causes

• Damage to brain centers involved in

sleep (hypothalamus, midbrain,

ascending reticular activating system)

• Disruption of circadian pacemaker in the

hypothalamus with decrease in level of

melatonin production

Sleep Disorders

Causes

• Pain

• Depression

• Anxiety

• Medications

• Environment

Sleep Disorders

Treatment • Treat depression, anxiety, pain

• Treat sleep apnea if present

• Improve sleep hygiene

• Melatonin

• Hypnotics, TCAs, antiepileptics may be helpful although no studies have shown best pharmacotherapy for insomnia in TBI

Fatigue

• The awareness of a decreased capacity

for physical and/or mental activity due to

an imbalance in the availability,

utilization and/or restoration of

resources needed to perform activity.

Fatigue

• Physiologic- arises from depletion of

energy, hormones, neurotransmitters, or

neural connections

• Psychologic- weariness related to

reduced motivation, prolonged mental

activity or boredom

Fatigue

• Kreutzer found 46% of 722 outpatients

with TBI self reported fatigue

Fatigue

• May result from diffuse neuronal injury,

particularly from damage to brain

centers that control arousal, attention

and response speed including the

ARAS, limbic system, anterior cingulate,

basal ganglia

• Alteration in chemistry. Histamine and

growth factor.

Fatigue

Fatigue

Treatments • Exercise

• Sleep assessment

• Hormonal screening

• Light therapy

• Assessment of meds. D/C meds that increase

fatigue

• Try antidepressants with activating effect

• Modafinil

Infections

• Meningitis

• Headache, fever, stiff

neck, confusion

Infections

• Subdural empyema

– Usually due to septic

skull fracture

– Acute presentation

with fever,

headache,

obtundation

Infections

• Brain abscess

– 3 times more likely with gunshot wound

– Usually 2-3 weeks post injury

– Headache, vomiting, change in mental

status 50%, seizure 33%

Craniectomy

• Syndrome of the

trephined

• Deficits that may

improve with

cranioplasty

– Headaches, apathy,

hemiparesis, tremor,

gait, cognitive

dysfunction

Trephination

Hydrocephalus

• Occurs in about 40% of patients with

severe TBI

• Usually begins to appear within the first

2 weeks post injury

Hydrocephalus

• Communicating

– Different portions of

the ventricular

system are

interconnected and

fluid may exit the

ventricular system

freely to the cisterns

and subarachnoid

space

Hydrocephalus

• Non-communicating

(obstructive)

– CSF flow is obstructed

either between the

ventricles or in exiting the

ventricular system

– Due to cerebral edema,

blood or infection which

interferes with CSF flow

– May present with

nausea, vomiting and

lethargy

Shunting

• Study of 356 adults with VP shunts over

18 years. Incidence of revision 30%.

• Shunt failure

• Shunt infection

• Overdrainage

VP Shunt

Shunt failure

• Proximal occlusion of the ventricular catheter is the most common source of blockage (30%)

• Disconnection of shunt components account for 15%

• Distal shunt obstruction due to encystment and loculation of peritoneal contents around distal tip

Shunt infection

• 70% present within the first 2 months

after shunt placement

• Low grade fever, malaise, irritability,

nausea, erythema over shunt site

Overdrainage

• Not seen as much with modern shunt

components (programmable valves)

• Orthostatic headache, dizziness,

nausea, lethargy, diplopia

• Can lead to chronic subdural hematoma

Overdrainage

Subdural hematoma

• Change in mental

status, signs of

increased

intracranial pressure

• Especially consider

in older patients

• Treatment is

neurosurgical; burr

hole or craniotomy

Epidural hematoma

• Due to injury of the

middle meningeal

artery

Spasticity

• Components of UMNS

– Spasticity

– Mass synergy patterns

– Weakness

– Loss of finger dexterity

Spasticity

• Rule out exacerbating factors

• Non-pharmacological treatments

• Oral medications

• Intrathecal baclofen

• Focal treatments

• Surgery

Neuroendocrine Dysfunction

• More common than once thought

• Autopsy study of 100 patients with TBI

found 62% had injury to pituitary

• Studies of hormone levels in patients

with severe TBI found 36-69% had

abnormal levels of at least 1 hormone

Pituitary Gland

Neuroendocrine Dysfunction

• All of the following have been reported abnormal in TBI survivors – Antidiuretic hormone

– Cortisol

– Growth hormone

– Thyroxine

– FSH/LH

– Prolactin

– Glucagon

– Somatostatin

Normal Pressure

Hydrocephalus • Classic triad- incontinence, gait disorder and

dementia

• Classic gait is short, wide based, magnetic steps

• Some believe this is the most common cause of post trauma HA – IGF1

– Urine assessment if polyuria

• Patients with moderate to severe TBI should undergo hormone evaluation at 3 months and 12 months post ICU discharge – Somatostatin

Neuroendocrine Dysfunction

• Recommendations of Global Experts

Consensus Panel 2005

• Patients with moderate to severe TBI

should undergo hormonal evaluation at

3 months and 12 months post ICU

discharge

Neuroendocrine Dysfunction

• Hormone evaluation should include – 9 AM cortisol level

– fT3, fT4

– TSH

– FSH

– LH

– Testosterone in males

– E2 in females

– Prolactin

– IGF1

SIADH

• Inappropriate ADH release will produce

hyponatremia by interfering with urinary

dilution and decreasing excretion of

ingested water

• Na < 135

• Nausea, fatigue, muscle cramps,

change in mental status, seizure, coma

Post Traumatic Headache

• Most common complaint after mTBI

• Consider causes such as hematomas, hydrocephalus, VP shunt malfunction

• Types – Musculoskeletal

– Cervicogenic

– Neuralgic

– Post traumatic migraine

– Post traumatic sinus headache

Musculoskeletal Headache

• Referred pain from muscles such as

trapezius and SCM

• Pattern often refers pain to retro or peri

orbital area

• Treatment with trigger point

management, acupuncture, postural

correction, meds

Musculoskeletal HA

Cervicogenic Headache

• Pain referred from

zygapophyseal

joints of c-spine

especially C2 and

C3

Neuralgic Headache

• Most common is greater occipital nerve

• Splenius muscle spasm or overactivity exacerbates

• Ipsilateral frontotemporal scalp

• Treatment with trigger point management, gabapentin, TCAs, NSAIDs, blocks, surgical decompression

Occipital Neuralgia

Post Traumatic Migraine

• Described as throbbing, unilateral, worse with

cough or bending over. May have visual

issues, nausea, vomiting

• Treatment like migraine in general population.

Prophylactic meds (NSAIDs, beta blockers,

calcium channel blockers, TCAs, depakote)

and abortive meds (triptans, ergot,

dihydroergotamine). Possible role for botox

Post Traumatic Sinus HA

• Patient with history of facial bone

fractures

• HA pattern may be based on drainage

angles

– Frontal and ethmoid worse with supine

– Maxillary and sphenoid better supine

Sinuses