2 Neuroscience2.10 Neurodevelopment and neuroplasticity

2.10.6 Effects of injury at different ages on the brain and mental function

Creator: Resident Doctor Committee
Published: 2026-10-14T21:05:16.259Z

3 min read2 figures

Written by Resident Doctor Committee · Published 14 October 2026

Injury at different ages

Feature	Childhood	Adult	Late life
Reorganisation	Greater after focal injury	Mainly through surviving networks	More constrained
Effect on function	Disrupts skills not yet emerged	Disrupts established skills	Reduces skills and reserve
Recovery	Later demands may reveal deficits	Greatest gains often within 6 to 12 months	Often slower

Growing into deficit is apparent early recovery after childhood injury giving way to difficulty as executive and social demands rise, especially after frontal injury.
Early focal injury can shift language to the opposite hemisphere, but diffuse early injury may disrupt development broadly despite greater plasticity.
Cognitive reserve falls with vascular disease, previous injury, alcohol and neurodegeneration. Education and occupational complexity serve as its proxies.

Traumatic brain injury

Contrecoup injury lies opposite the impact and coup injury lies beneath it, so a blow to the back of the head bruises the frontal pole.
The basal frontal (orbitofrontal) surface is the most vulnerable, and injury there gives disinhibition and personality change.
Diffuse axonal injury is rotational shear of white matter, corpus callosum and brainstem, and computed tomography may miss it.
Sequelae include slowed processing, memory and executive problems, depression, apathy and irritability. The duration of post-traumatic amnesia predicts outcome.
Traumatic brain injury raises the risk of non-affective psychosis more than that of affective psychosis, and it is linked with epilepsy and dementia.

Side view of a skull and brain hitting a fixed object at the forehead, with arrows showing the brain moving forward and back inside the skull. Red bruising is labelled coup injury at the front and contrecoup injury at the back. — The fixed object strikes the front of the head, so coup injury lies beneath the impact at the frontal pole and contrecoup injury lies opposite it at the occipital pole. Patrick J. Lynch, medical illustrator, CC BY 2.5, via Wikimedia Commons

Chronic traumatic encephalopathy

Chronic traumatic encephalopathy (dementia pugilistica) follows cumulative repetitive head impacts over years, and that history supports the diagnosis.
Comparable pathology has also been described after a single brain injury.
Martland gave the first medical account in 1928 and named it 'punch drunk'. Millspaugh's term 'dementia pugilistica' came nine years later.
Diagnosis needs post-mortem confirmation.
The pathognomonic lesion is hyperphosphorylated tau in neurones clustered around small blood vessels at the depths of cortical sulci.
A fenestrated cavum septum pellucidum is a post-mortem marker. Its leaflets are torn by repeated impact and by ventricular stretch.

Two tau-stained sections of cortex with brown staining on a blue background. On the left, at low power, brown patches sit at the bottoms of cortical folds. On the right, at higher power, brown-stained cells cluster around two small vessels, each marked with an arrow. — At low power (A) the brown hyperphosphorylated tau lies at the depths of the cortical sulci, and at higher power (B) it clusters around small blood vessels, which is the pathognomonic lesion of chronic traumatic encephalopathy. Priemer DS et al. JAMA Netw Open. 2025;8(6):e2517686, Figure 1A and B. CC BY 4.0

Multiple sclerosis

Multiple sclerosis causes multifocal demyelinating plaques in the brain, optic nerves or spinal cord, so its features depend on where the lesions lie.

Diagnosis needs demyelinating lesions of the central nervous system disseminated in time and in space. This means relapsing multifocal symptoms, and magnetic resonance imaging lesions of different ages in more than one typical region.
It usually starts in young adulthood, often at 20 to 40, and prevalence rises with distance from the equator.
Risk factors include Epstein-Barr virus, low vitamin D and smoking.
Optic neuritis is demyelination of one optic nerve and is the typical ocular presentation. It causes subacute monocular visual loss, often with pain on eye movement.
About 85% of cases begin relapsing-remitting. The other 10 to 15% are primary progressive and worsen steadily from onset.
Most untreated cases progress to disability.
Depression is the commonest psychiatric disorder in multiple sclerosis. Fatigue is common and is distinct from depression, and steroids can cause mood change or psychosis.

Encephalitis, sarcoidosis and hydrocephalus

Condition	Features
GABA-B (gamma-aminobutyric acid B) receptor encephalitis	Limbic encephalitis with memory loss, confusion, behavioural and mood change, and seizures; sometimes small cell lung cancer
GABA-A receptor encephalitis	Heavier, more treatment-resistant seizures than GABA-B, with refractory seizures and status epilepticus
Neurosarcoidosis	Neuropsychiatric symptoms with systemic signs in skin or lung; non-caseating granulomas with asteroid bodies

Normal pressure hydrocephalus gives a triad of gait, bladder and cognitive disturbance without raised intracranial pressure.
Obstructive hydrocephalus raises intracranial pressure, which causes headache, vomiting, bradycardia and papilloedema.

Brain tumours

Brain tumours act through infiltration, oedema, raised pressure and seizures.
Frontal tumours cause apathy or disinhibition.
Temporal tumours cause seizures, amnesia or psychosis.

Revision material for the MRCPsych examinations. Not clinical guidance, and not for use in patient care.