Brain injury

• 1. Introduction

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  A tamping iron tore through Phineas Gage's frontal lobe in 1848 while he paved a new railroad line, and he survived. He kept his functional abilities, yet the friendly, respectful man his physician John Martyn Harlow had known became rude, inconsiderate and indecisive. This is brain injury: the destruction or degeneration of brain cells. It arrives from a blow, a burst vessel, an infection, a toxin, a faulty gene. What decides whether someone walks away, loses their words, or never wakes? Why can one person recover speech while another keeps a permanently altered personality? And how did physicians across thousands of years learn to read the damage hidden inside a living skull?

• 2. Mapping The Damage

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  Focal brain injuries strike a single area, born of direct force, surfacing as haemorrhages, contusions and subdural and epidural haematomas. Diffuse injuries spread across all or many regions, driven by diffuse axonal injuries, hypoxia, ischaemia and vascular injuries. When both are severe, the focal kind is deadlier, with a mortality rate of 40% against 25% for diffuse injuries. The diffuse kind, though, more often leaves long-term neurological and cognitive deficits behind.

  Primary injuries happen at the instant mechanical forces deform the brain. Secondary injuries develop afterward from conditions like hypoxia, ischaemia, oedema, hydrocephalus and intracranial hypertension, which may or may not follow the primary blow. Doctors also sort severity into three categories: mild, moderate and severe. A mild injury caused by a blow to the head is a concussion, and its quiet signature of headaches, tinnitus, fatigue and shifting sleep can go unrecognised. Acquired injuries occur after birth, set apart from the congenital injuries some patients carry from the very beginning.

• 3. When The Self Changes

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  Wernicke's aphasia robs a person of word retrieval, fills their speech with invented words called neologisms, and breaks their grasp of language, all from damage to the posterior section of the superior temporal gyrus. Damage to Broca's area instead strips out functional words, alters sound production, and brings alexia and agraphia from harm to the posterior inferior frontal gyrus. A lesion to the fusiform gyrus can cause prosopagnosia, the inability to tell faces and complex objects apart. Lesions to V4 can cause colour-blindness, and bilateral lesions to MT/V5 erase the ability to perceive motion.

  Pure alexia shows how tangled this mapping can be. A lesion damaging both the left visual field and the connection between the right visual field and the language areas destroys reading, yet the person can still write, speak, and even transcribe letters without understanding them. Emotional changes follow too, sometimes sudden mood swings that subside as fast as they came, untriggered by any event. Brain injuries raise the risk of depression, bipolar disorder and schizophrenia, with the correlation strongest in female and older patients. Any acquired injury can shift the Big Five traits, raising neuroticism while lowering extraversion and conscientiousness, until a patient aware of the change feels cut off from who they used to be.

• 4. The Many Doors To Harm

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  A coup injury sends the brain against the side of the cranium that struck the object, while a contrecoup injury makes the brain bounce back and strike the opposite side, the more severe of the two. Diffuse axonal injuries come from shearing forces in events like traffic accidents, where sharp rotational acceleration tears the brain's white matter tracts. Penetrating head trauma from gunshot wounds and stabbings is the most lethal form of traumatic brain injury, killing 70-90% of victims before they reach the hospital. Blast injuries split into primary, secondary, tertiary and quaternary, with wounds close to the epicentre largely fatal and distant ones often mild or moderate.

  Haemorrhagic strokes burst a blood vessel so blood leaks around the brain and raises intracranial pressure, while ischaemic strokes choke off circulation until starved brain cells die. Huntington's disease passes down in an autosomal dominant pattern, traced to a mutation on the short arm of chromosome 4p16.3 that lets the Huntingtin protein aggregate, with symptoms usually arriving between ages 30 and 50. In Parkinson's disease, falling dopamine unbalances the basal ganglia, and 70 to 89% of patients face symptoms like depression, anxiety and dementia. Brain tumours can grow in place or spread from lung cancer, breast cancer and melanoma, and most cases are in fact metastatic.

• 5. Poisons And Deficiencies

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  Mercury, common in manufacturing yet detrimental to neurological health, atrophies the cerebellum, the postcentral gyri and the calcarine sulcus when it deposits in the central nervous system. Children exposed to high doses of methylmercury, or whose mothers were exposed during pregnancy, are far likelier to have intellectual disabilities, cerebral palsy, developmental delays and epilepsy. Lead was banned from gasoline in the United States in 1972 and from paint in 1978, but it still binds to proteins throughout the body and disrupts the synaptic pruning that children undergo. In extreme doses it brings lead encephalopathy, with cerebral edema, seizures, coma and death.

  Wernicke-Korsakoff syndrome stems from a deficiency of vitamin B1, also called thiamine, and unfolds in two stages. Wernicke's encephalopathy comes first, born of focal lactic acid accumulation that disturbs vision, coordination and balance. Korsakoff psychosis tends to follow as those symptoms fade. The deficiency itself traces to causes like chronic heavy alcohol use, or to conditions affecting nutritional absorption such as colon cancer, eating disorders and gastric bypass. Chemotherapy adds its own toll, damaging neural stem cells and the oligodendrocyte cells that produce myelin, an effect commonly called chemo brain.

• 6. Reading The Living Brain

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  The Glasgow Coma Scale rests on three traits: whether a person can open their eyes, speak coherently, and follow a command to move. Eye opening is worth 4 points, speech 5 and motor ability 6, so severe injuries score 3 to 8, moderate ones 9 to 12, and mild ones 13 to 15. A patient is intubated if their score drops below 8, or if they show severe facial fractures, severe hypertension, or signs of transtentorial herniation. CT scans and MRI are the two most effective and widely used imaging techniques. CT reveals haemorrhages, skull fractures and fluid buildup, while MRI catches smaller injuries, diffuse axonal injuries and damage to the brainstem and posterior fossa, though pacemakers and metal implants rule it out.

  Emergency care guards the brain's oxygen supply and keeps blood pressure normal to prevent further injury, and a catheter set into a ventricle can monitor intracranial pressure to guide decisions. Corticosteroids like dexamethasone, cortisone and prednisone lower that pressure, while mannitol may be given for herniation or neurological deterioration. Surgery is rarely required for traumatic brain injuries because most are mild. Epidural and subdural haematomas, though, must be evacuated to prevent herniation and death, done through a decompressive craniectomy that leaves the skull section out, or a craniotomy that replaces it.

• 7. The Brain That Rebuilds

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  Neuroplasticity lets the brain partially recover by forming new neural connections to compensate for damaged areas, so patients may regain movement and speech, especially with therapy and practice. Areas of the brain can learn to cover for damaged ones, growing in size and complexity and even changing function, much as someone who loses a sense gains sharper acuity in another. Neuroregeneration comes more easily in the peripheral nervous system and is far rarer in the central nervous system of the brain and spinal cord. A common misconception holds that brain damage means recovery is impossible, yet returning to pre-injury function, while not guaranteed, is not out of reach.

  Physiotherapy in the post-acute phase may include sensory stimulation, serial casting and splinting, fitness and aerobic training, and functional training. The evidence is uneven: there is none supporting sensory stimulation, and no studies back sit-to-stand training, arm ability training or body weight support systems. Serial casting, however, can increase passive range of motion and decrease spasticity. Adults aged 60 or older tend to face worse outcomes, longer comas and slower recovery, even from an equivalent injury, because of age-related changes and reduced physiological reserves. A child's frontal injury can hide its damage until they fail to develop normal executive functions in their late teens and early twenties.

• 8. Centuries Of Witness

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  The Edwin Smith Papyrus of Ancient Egypt, written in the 16th century BC, first recorded that injuries to the meninges stiffened the neck, that lesions of the cerebrum brought paralysis, and that temporal lobe damage caused aphasia. It advised rubbing grease across the injury, dressing open wounds when the skull was not fractured, and keeping the patient upright. In Ancient Greece, Hippocrates, Celsus and Galen noted that head injuries were often followed by lost consciousness. Centuries later, in 1825, the French physician Jean-Baptiste Bouillaud proposed that frontal lobe lesions disturbed speech, though he missed that the localisation was left-sided.

  Paul Broca met a patient named Louis Victor Leborgne in 1861, a man who could utter only the syllable tan. Leborgne died the same year, and the autopsy revealed a lesion in his left frontal lobe. A second patient, Lazare Lelong, could speak only five words, and his autopsy showed the same left frontal damage. In 1874, Carl Wernicke described a stroke patient who could hear and speak but could no longer comprehend language, traced after death to a lesion in the left temporal region. In 1928, the pathologist Harrison Martland reported on punch drunk boxers who developed dementia and Parkinsonian symptoms, and in 1940 Abram Blau and Karl Murdoch Bowman renamed it chronic traumatic encephalopathy after a 28-year-old boxer with psychosis.