Medical Complications in Traumatic Brain Injury

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Medical and neurological complications determine the final functional outcome, community reintegration as well as vocational potential after TBI. Therefore, it is important to recognise the potential risks of those pathologies and to follow the evidence based efficient protocols minimising the risk of secondary complications. Timed implementation of therapeutic approaches to reduce resultant impairment should concentrate on reducing the extend of the complications. 

The long-term physical, cognitive, and behavioural complications are related to the direct brain injury but also to the influence of central nervous system disfunction and trauma on other organs and system. Several complications can occur immediately or soon after a traumatic brain injury, but some might not be recognised until rehabilitation stage. Severe injuries increase the risk of a greater number and more-severe complications.

Presence of the complications and the injury related impairment impacts the quality of life of person living with TBI. These problems can cause frustration, conflict and misunderstanding of people with a TBI as well as family members or friends. [1] Individual’s risk of suicide as well as mood and anxiety disorder might be increased due to combination of symptoms and neuropsychiatric factors often aggravated by the trauma.

Medical Complications

Medical complications include:


TBIs involving skull fractures or penetrating wounds can result in meninges damage. This can result in bacterial brain infection. An infection of the meninges (meningitis) could spread to the rest of the nervous system if not treated.

Sepsis, or multiple organ dysfunction syndrome are the leading causes of late morbidity and mortality in TBI. The catecholamine surge following systemic insult is directly involved in the regulation of cytokine expression in situations of acute stress producing a worsening clinical condition and, ultimately, a poor outcome. The trauma-induced catecholamine surge affects systemic organs and contributes to organ damage. [2]


One of the upper motor neuron syndrome features developing rapidly in some cases as early as one week post TBI, often resulting in orthopaedic sequalae. [3] The mild spasticity can have some benefits like maintaining muscle bulk or enhancing gait, but moderate to severe muscle tone increased and spasm severely impact rehabilitation outcomes, functional recovery and ability to engage in activities of daily living. Moderate to severe spasticity require structured management protocols [redirect to future contracture management topic]

Venous Thromboembolism

Venous thromboembolism is a condition when cloth is formed in limbs deep veins and after ending in circulation system enters the lungs causing pulmonary embolism which is a direct life-threatening condition. After TBI incidence is as high as 54% due to difficulties using anticoagulation in acute post TBI period. The VTE prophylaxis can be applied only after the risk of renewed intracranial haemorrhage decreases.

Paroxysmal Sympathetic Hyperactivity (PSH)

Sympathetic hyperactivity similar to “the storm after TBI, observed for week or months and presenting with increased sympathetic activity: heart rate increase, blood pressure increase, respiratory rate increase, sweating, hyperthermia, motor posturing. [4] The PSH is related to poor outcome and results from disconnection syndrome following impairment of inhibitory control over excitatory autonomic centres.

Neuroendocrine Dysfunction / Post TBI Hypopituitarism

Clinically prevalent phenomenon related to damage of the pituitary gland, a small gland that sits at the base of the brain and regulates other endocrine glands, i.e.: thyroid, adrenal glands, pineal gland. Damage to pituitary gland is more prevalent in cases with skull fracture and affects its own function as well as affects other hormones production and impacting the homeostasis metabolism, mood, growth, sleep and other bodily functions. The hypopituitarism has been related to presence of depression and fatigue. Resultant thyroid malfunction to neuropsychiatric issues, cardiac function decrease, anxiety, diabetes insipidus. 

Heterotopic Ossification (HO)

Incidence of 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification. It presents with abnormal formation of ectopic lamellar bone in soft tissue. The HO tends to form around the bigger joints  like hip, knee, shoulder and causes range of motion decrease with limited mobility, pain, decreased function. Timely prophylactic with nonsteroidal anti-inflammatory drugs and imaging modalities diagnostic should b implemented early to prevent severe mobility impairment. Other approaches include use of bisphosphonates (not clearly evidence), radiation and physiotherapy allowing mechanical improvement. Fully formed HO can be surgically excised when sever pain or lose of range of motion impact mobility or personal care.

Bladder Bowel Dysfunction and Genitourinary Complications

Among the most common sequelae in patients with TBI due to ineffective communication, cognitive deficits, behavioural difficulties. Urinary disfunction relates to detrusor overactivity and often to longer stay at acute services and delayed rehabilitation. At discharge those patients demonstrate poorer functional recovery. Establishing the causes, i.e.: urinary tract infection, optimal medication usage and pelvic floor exercises improve the outcome. 

Neurogenic bowel can be either incontinence or constipation. Even 68% admitted to rehabilitation might demonstrate faecal incontinence. Hydration, fibres intake, medication or toilet training help. Untreated bladder and bowel dysfunction impose a risk on tissue viability. 

Sexuality impairment related to frontal lobe damage, limbic system malfunction might present as hypersexuality, decreased sexual drive, lack of satisfaction or ejaculation disfunction. Social and intimacy difficulties aggravate the sexual malfunctions. Resultant inappropriate sexual behaviour creates potential risks of difficulties forming relationships, aggression and criminalisation.

Nutritional Deficits 

Endocrine and inflammatory processes after TBI relate to excessive energy expenditure and consequent malnutrition, hyperglycaemia, hypercatabolism of proteins, lack of wound healing, muscle waiting and urinary nitrogen excretion. Enteral feeding with heavy protein supply can improve outcomes. Optimal nutrition facilitates better sleep behaviour, physical fitness, emotional status, fatigue management.

Sleep Disturbances

Extremely common complication amongst people living with TBI. Include insomnia, hypersomnia, excessive daytime sleeping and impaired circadian sleep-wake pattern. [5] The pathology depend on the injured area and could be treated with sleep hygiene training, daytime exercises, caffeine intake limitation, CBT and medication.

Posttraumatic Headache

Commonly present after TBI; tension-type headaches are the most common form, but exacerbations of migraine-like headaches are also frequent. Often long-term problem.

Neurological Complications

Neurological complications include:

Post-traumatic Seizures

Post-traumatic Seizures frequently occur after moderate or severe TBI. They may occur only in the early stages, or years after the injury (post-traumatic epilepsy). The post injury classification is:  

  • Immediate Seizures (occurring within 24 h after injury) 
  • Early Seizures (occur less than 1 week after injury) 
  • Late Seizures (occur more than a week after injury).  

Risk Factors include:  

  • Bilateral contusion 
  • Dural penetration 
  • Subdural hematoma 
  • Multiple intracranial surgeries 
  • Midline shift > 5mm 
  • Presence of severe injury measured by GCS.  

The posttraumatic seizure relates to poor functional outcome. Phenytoin and levetiracetam are the most commonly used drugs in prevention and treatment of seizures. 


Cerebrospinal fluid may build up in the cerebral ventricles causing increased pressure and swelling in the brain. As much as 70% of patients demonstrate ventricular enlargement 2 months post moderate to severe TBI. Craniectomy, severe TBI, older age, longer come, intracranial bleeding are possible risk factors. In rehabilitation plateau or functional decline might suggest the presence of post-traumatic hydrocephalus (PTH). Clinically a patient developing PTH might demonstrate headache, nausea, urinary incontinence, cognitive decline, papilledema, motor impairment. Imaging diagnostic extended by lumbar puncture are usual diagnostic tools with shunt placement being the treatment option. 

Cranial Nerves Disorders

TBI at the base of the skull can cause damage to the nerves that emerge directly from the brain or brainstem. Cranial nerve damage may result in: 

  • Paralysis of facial muscles or losing sensation in the face
  • Loss of or altered sense of smell
  • Loss of or altered sense of taste
  • Loss of vision or double vision
  • Swallowing problems
  • Dizziness
  • Ringing in the ear
  • Hearing Loss

Visual Dysfunction

Visual Dysfunction may present as blurred vision, sensitivity to light, reading difficulty, headaches with visual tasks, reduction or loss of visual field like hemianopsia, and difficulties with eye movements, gaze stabilization deficits. The visual problems impact on other areas of functioning like communication, mobility and balance. They also impact on safety, i.e.: visual field defects.

Neurosensory Deficit 

May include somatosensory loss, persistent ringing in the ears, difficulty recognizing objects, blind spots or double vision, bitter taste, a bad smell or difficulty smelling, paraesthesia like skin tingling, itching, numbness or pain. The array of problems requires careful assessment to inform the most effective treatment as untreated the neurosensory deficits impact on other components like motor control and final level of functional recovery.

Spatial Neglect

Spatial Neglect is a complex problem involving perception, movement and memory presenting as impaired attention to the side contralateral to the lesion. Presence of unilateral neglect severely impairs the recovery. Therapeutic approaches should include motor, sensory and compensatory strategies teaching, however there is no sufficient evidence of clinical effectiveness or superiority of any approach.

Movement Disorders

Movement disorders can be demonstrated as hypokinetic or hyperkinetic phenomenon and might present as: tremor, chorea, dystonia, athetosis, ballism, myoclonus, parkinsonism, tics. [5] The movement disorder might be the only symptom or coexist with other movement or motor disorders. They can also be a side effect from medication used to treat for example impaired cognition or arausal. Some pathologies like dystonia occur in acute phase post TBI, but some like parkinsonism can occur decades after the trauma. The most common movement disorder after TBI are tremors, dystonia, parkinsonism, myoclonus and are more prevalent in individuals post a severe injury more moderate to mild injury. The areas of the brain often involved in movement disorder are: basal ganglia, cerebellum, thalamus, subthalamus, white matter tracts. Treatment include elimination of the cause, i.e.: haematoma or hydrocephalus; pharmacological and surgical interventions.

Dizziness / Balance Disorders

Dizziness and balance disorders are a common TBI complication with dizziness being reported by 80% of people. The aetiology might be complex including vestibular impairment, sensory integration problems, visual or proprioceptive. Main pathologies include BPPV, central vestibular or peripheral problem, like vestibular nerve damage or injury to semi-circular canals. Physiotherapeutic treatment depends on the pathology aetiology. 

Sleep / Wake Disorders

Post TBI the restorative function of sleep is diminished, and the sleep pathology is very common. Contributing factors include biochemical and structural changes to the brain especially reticular system, thalamus and hypothalamus, environmental like no clear day/night time at the hospital ward, medicinal like pain and behavioural like naps during the day or caffeine intake. Sleep hygiene training have some effectiveness with pharmacological substances like melatonin, benzodiazepines or zolpidem, exercises or light therapy also used. 


Fatigue in people with TBI is of central nature causing cognitive tasks more difficult and peripheral causing musculoskeletal tiredness. The fatigue presence has got negative impact on rehabilitation participation. Basal ganglia are often involved. The treatment includes environmental adjustments and sometimes medication like modafinil.

Behavioural & Emotional

Behavioural and emotional changes including agitation, difficulty with self-control, lack of awareness of abilities, risky behaviour, verbal or physical outbursts, alcohol misuse, binge drinking, anxiety and depression, mood swings, irritability, anger, lack of empathy for others. All those can heavily affect rehabilitation outcome and community reintegration.  The behavioural changes might have destructive impact on relationship, vocational potential or criminal engagement. Neuropsychologist and neuropsychiatrist are integral part of the MDT working with people after brain injury and challenging behaviour management programmes integrated and followed by all professionals and relative involved. Posttraumatic depression is further associated with cognitive decline, anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts.

Cognitive Decline

Following areas can be affected and impact on information processing, communication, movement execution and balance skills:

  • Memory: Sensory memory, working memory, short term, long term, semantic memory, procedural memory, episodic memory 
  • Learning new skills and information
  • Reasoning
  • Judgment
  • Attention or concentration
  • Executive functioning problems
  • Problem-solving
  • Multitasking
  • Organization
  • Planning
  • Decision-making
  • Beginning or completing tasks

Degenerative Brain Diseases and Dementia

Often resulting from repeated or severe traumatic brain injuries; People living with TBI are at approximately 4 times greater risk of developing dementia and earlier in life comparing to general population. Repetitive injures have been related to Chronic Traumatic Encephalopathy (CTE) or Dementia Pugilistica (“Boxer’s Dementia) whilst single brain injury has been related to Alzheimer’s type symptoms. The exacerbation of degenerative brain diseases following TBI is related to genetic background. 

Altered Consciousness

Results from moderate to sever TBI, relates to changes in person’s state of consciousness, awareness or responsiveness. Different states of consciousness include:

  1. Coma: A person in a coma is unconscious, unaware of self and environment and unable to respond to any stimulus. This results from widespread damage to all parts of the brain. The person with TBI may emerge from a coma or enter a vegetative state at various time after the trauma.
  2. Vegetative State (VS): Related to widespread damage to the brain. The person is unaware of surroundings, but might open eyes, make sounds, respond to reflexes or move. The person can remain in VS permanently, but some patients can make a transition to a minimally conscious state.
  3. Minimally Conscious State: A condition of severely altered consciousness but with some signs of self-awareness or awareness of an environment. It is sometimes an intermittent state between coma or VS and some degree of consciousness recovery.
  4. Brain Death: Is declared when there is no measurable activity in the brain and the brainstem. In a person who has been declared brain dead, removal of breathing devices will result in cessation of breathing and eventual heart failure. Brain death is considered irreversible.

Communication Deficits

Communication deficits of various nature including:

  • Difficulty understanding speech or writing
  • Difficulty speaking or writing
  • Inability to organize thoughts and ideas
  • Trouble following and participating in conversations
  • Trouble with turn taking or topic selection in conversations
  • Problems with changes in tone, pitch or emphasis to express emotions, attitudes or subtle differences in meaning
  • Difficulty understanding nonverbal signals
  • Trouble reading cues from listeners
  • Trouble starting or stopping conversations
  • Inability to use the muscles needed to form words (dysarthria)


  1. 26.05.2019
  2. Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. Journal of Intensive Care. 2016. 4:29-39. DOI 10.1186/s40560-016-0138-3
  3. Bose P, Hou J, Thompson FJ. Traumatic Brain Injury (TBI)- Induced Spasticity: Neurobiology, Treatment, and Rehabilitation. In: Kobeissy FH, editor. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton: CRC Press/Taylor & Francis; 2015. Chapter 14.
  4. Meyfroidt G, Baguley DJ, Menon DK. Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. The Lancet Neurology. 2017. 16(9):721-729.
  5. 5.0 5.1 Eapen BC, Cifu DX. Editor. Rehabilitation After Traumatic Brain Injury. Elsevier2018