Following brain injury, the person may in subsequent months or years develop additional complications which affect cognitive functioning. There are a number of potential causes of reduced cognitive functioning following brain injury and a comprehensive assessment is therefore required.
Epilepsy
Seizures occur after 5% of closed and 30% of open head injuries. These may develop during the first year following brain injury or later. If the person experiences tonic-clonic seizures they may be observed to exhibit a deterioration in cognitive functioning, particularly in the post-ictal phase (i.e. following the seizure).
Non-convulsive or nocturnal seizures may not be observed and therefore can be missed. However it is important to recognise that this may be a cause of a deterioration in cognitive functioning.
Accurate diagnosis is important and specialist advice should be sought from a Consultant Neurologist, with a view to considering the most appropriate antiepileptic medication.
Hydrocephalus
Hydrocephalus occurs in around 15% of individuals after severe traumatic brain injury (see reference below). In a substantial number of individuals hydrocephalus develops after the acute period of care (i.e. weeks or months later during the rehabilitation period or following discharge). Symptoms include headache, signs of raised intracranial pressure, shuffling, slow or ataxic gait. A deterioration in cognitive function may be observed. Treatment involves neurosurgical assessment and placement of either a ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt. Shunt blockage can occur at any time after its initial placement. This results in recurrence of hydrocephalus with the same associated clinical features.
Ref: (Kammersgaard LP, Linnemann M, Tibæk M. Hydrocephalus following severe traumatic brain injury in adults. Incidence, timing, and clinical predictors during rehabilitation. NeuroRehabilitation. 2013 Jan 1;33(3):473-80).
Central Nervous System (CNS) Infection
CNS infection can occur acutely after open head injury. Beyond the acute period and after recovery from any neurosurgical procedures, the person with an indwelling ventricular shunt for hydrocephalus remain at increased risk of infection of cerebrospinal fluid (CSF), especially in the first six months. Signs and symptoms of CNS infection include headache, drowsiness, vomiting, and ultimately signs of sepsis. Changes in cognitive functioning are observed, varying from subtle deterioration to delirium (i.e. acute onset of severe confusion associated with changes in mental state).
Autoimmune Encephalitis
Autoimmune encephalitis refers to a range of neurological disorders identified in recent years, the cause of which is not yet fully understood. These disorders are thought to arise from the development of antibodies to the person’s own CNS proteins. These antibodies act against CNS:
- Membrane receptors e.g. NMDA (N-methyl-D-aspartate) receptors.
- Ion channel associated proteins (e.g. voltage-gated potassium channels).
Autoimmune encephalitis presents with a wide range of neurological and neuropsychiatric features: which may include alteration in consciousness, cognitive deterioration, movement disorders and seizures. This condition may present in acutely or in a more insidious manner and may include the following clinical features:
- Alteration in level of consciousness.
- Cognitive deterioration.
- Behavioural changes including disinhibition.
- Deterioration of communication ability.
- Movement disorders (dystonia e.g affecting eyes, mouth, neck, trunk, arms and legs).
- Changes in hearing, vision and perception.
- Seizures.
- Psychiatric symptoms (e.g. hallucinations, delusions).
- Changes to sleep pattern.
- Bladder and bowel dysfunction.
- Changes in blood pressure, heart rate and breathing.
Where there has been a breach in the blood-brain-barrier (including post traumatic brain injury), antibodies to the NMDA receptor are more likely to be found. This may be as a result of the immune system being exposed to brain proteins which are usually hidden behind the blood-brain-barrier.
The consequence is NMDA receptor encephalitis, although it seems likely that such individuals may also be at increased risk of other types of autoimmune encephalitis via the same mechanism.
