MSC Neuro 25 p2

Severe: contusion/DAI/compression, GCS 4–7, coma with life-threatening systemic involvement.

44, 45. Clinical forms of traumatic brain injury. Concussion of the brain. Syndromology, course, treatment. Brain injury, diffuse axonal injury. Pathogenesis, clinic, diagnosis, care.

Clinical Forms ofTraumatic Brain Injury (TBI)

1.Concussion of the brain (Commotio cerebri)

Pathogenesis:

Mild closedTBI.

No neuronal death → only reversible axonal disconnection (functional break).

Caused by rapid CSF movement → impact on ventricular walls (reticular formation affected).

Clinical features:

Short LOC (seconds–30 min). May be absent.

Amnesia: retrograde / anterograde.

Headache, dizziness, nausea, single vomiting, unsteady gait.

No focal neurological deficits – only general cerebral symptoms.

Sleep and memory disturbances possible (drowsiness → insomnia).

Symptoms last 7–10 days, fully reversible.

Investigations:

CT – cerebral edema, blurring of brain structures, ventricular narrowing.

CSF: clear, no blood; pressure slightly ↑.

Skull X-ray, EchoEG → to rule out fracture / hematoma.

Treatment:

Bed rest 10–14 days.

Analgesics (for headache).

Antihistamines (Diphenhydramine – for vomiting, sleep).

Vegetative stabilizers (Bellataminal).

Nootropics (Piracetam,Aminalon).

Diuretics if ↑ICP.

Prognosis: Work capacity restored in ~2 weeks, but late complications (psychic issues, post-concussion syndrome) possible.

2.Brain Contusion (Contusio cerebri)

Pathology: Structural brain damage with neuronal death, edema, hemorrhage.

Types (by severity):

a.Mild Contusion

LOC: few minutes – 30 min.

Retro/anterograde amnesia.

Symptoms: Headache, dizziness, nausea, vomiting (sometimes repeated).

Minor neuro deficits (nystagmus, anisocoria, pyramidal signs, meningeal signs).

Regress in 2–3 weeks. May have skull fractures, SAH.

b.Moderate Contusion

LOC: tens of minutes – hours.

Severe headache, repeated vomiting.

Amnesia more pronounced.

Transient vital disturbances (tachy/bradycardia, ↑BP, tachypnea).

Focal signs: paresis, speech disorder, sensory loss, oculomotor/pupillary abnormalities.

Recovery: 2–5 weeks; may leave residual deficits.

c.Severe Contusion

LOC: hours – weeks (coma).

Gross brainstem signs: eye movement disorders, gaze paresis, dysphagia, bilateral reflex changes, decerebrate rigidity.

Severe vital disturbances: respiratory, cardiovascular, thermoregulation failure.

High risk of seizures, paralysis, gross residual disabilities. Often skull fractures + massive SAH.

Treatment:

Acute: airway, breathing, circulation support; anti-shock therapy.

Dehydration therapy: Mannitol, furosemide, glycerol.

Glucocorticoids: Dexamethasone, Prednisolone.

Symptomatic:

Headache → analgesics

Vomiting/dizziness → antihistamines, Cinnarizine, Diphenhydramine

Agitation/insomnia → tranquilizers, barbiturates

Nootropics + vitamins (Piracetam,Aminalon, Pantogam).

Rehabilitation: massage, physiotherapy, speech therapy.

3.DiffuseAxonal Injury (DAI)

Pathogenesis:

Rapid acceleration/deceleration → axonal stretching & rupture (e.g. car accident, fall, shaken baby syndrome).

Microhemorrhages in corpus callosum, semioval center, upper brainstem.

Clinical features:

Deep prolonged coma immediately after trauma.

Vegetative state (no cortical activity, preserved autonomic).

Vital dysfunction: fluctuations in BP, respiration, temperature.

Poor recovery, often persisting vegetative state for months/years.

Diagnosis:

CT → generalized brain edema, compression of basal cisterns, small subcortical lesions.

Clinical: Coma + absence of focal dominance → DAI suspicion.

Treatment:

Supportive, as surgery is ineffective.

Maintain airway, oxygenation, perfusion.

Prevent ↑ICP (mannitol, hyperventilation, head elevation).

Prolonged ICU care.

High morbidity and mortality.

Takeaway for exams:

Concussion = reversible functional TBI.

Contusion = structural brain lesion, graded mild/moderate/severe.

DAI = severe disconnection syndrome with coma → vegetative state.

46.Traumatic brain compression. Mechanisms. Intracerebral traumatic hematomas. Syndromology. Treatment.

Traumatic Brain Compression (CCM)

Definition

A progressive pathological process inside the skull caused by space-occupying lesions (hematomas, depressed fractures, hygromas, pneumocephalus, crush injuries), which overwhelm compensatory mechanisms → lead to dislocation & brainstem herniation (life-threatening).

Occurs in ~3–5% ofTBI cases.

Mechanisms (Etiology & Pathogenesis)

1.Increasing Compression (progressive growth):

Epidural, subdural, intracerebral, intraventricular hematomas

Brain contusion/crushing with mass effect

2.Non-increasing Compression (static, but with secondary edema):

Depressed skull fracture fragments

Foreign bodies, pneumocephalus, focal crush injury

Pathogenesis:

Hematoma/foreign body → volume expands → ↑ICP→ edema → collapse of ventricles/basal cisterns → displacement of midline structures (>5 mm) → herniation syndrome.

Syndromology (Clinical Picture)

Symptoms appear immediately or after a “light interval”.

General cerebral:

↓ Consciousness (stunning → coma), headache, repeated vomiting, psychomotor agitation.

Focal:

Hemiparesis, unilateral mydriasis (fixed dilated pupil on side of lesion), partial seizures.

Brainstem:

Bradycardia, hypertension (Cushing’s triad), tonic nystagmus, gaze palsies, bilateral pathologic signs.

Forms of Traumatic Hematomas

1.Epidural Hematoma

Source: Middle meningeal artery tear (most common), sinus bleeding.

Course:

LOC → light lucid interval → deterioration.

Ipsilateral fixed dilated pupil.

Contralateral limb paresis.

Late: decerebrate rigidity, bradycardia, hypertension.

Treatment:

Emergency trepanation/osteoplastic craniotomy.

Hematoma evacuation (suction, saline wash).

Stop bleeding: coagulation/ligation of meningeal artery, control sinus/diploic bleeding.

2.Subdural Hematoma

Source: Bridging veins (parasagittal region), brain vessels after contusion.

Types:

Acute (hours–1–2 days): severe, rapidly progressing.

Subacute (4–14 days): symptoms rise while acute TBI subsides.

Chronic (weeks–months): encapsulated, common in elderly/alcoholics; often after trivial trauma.

Clinic:

Progressive headache, confusion, focal neuro signs, hemiparesis, seizures.

Treatment:

Acute/subacute → craniotomy + evacuation.

Chronic → burr hole drainage with catheter; avoid rapid emptying (risk of rebleed).

3.Intracerebral Hematoma

Blood clots + detritus within brain parenchyma (frontal/temporal lobes common).

Symptoms: focal signs depend on location (hemiplegia, speech deficit, seizures), general deterioration.

Treatment: surgical removal if large/symptomatic; conservative if small and stable.

4.Subarachnoid Hemorrhage (SAH,TBI-induced)

Mechanism: Rupture of arteries, aneurysms, or trauma → bleeding into subarachnoid space.

Clinic: sudden “thunderclap headache,” repeated vomiting, LOC, agitation.

Treatment:

Secure airway, ventilation if needed.

BPstabilization.

Prevention of vasospasm: Nimodipine (Ca-channel blocker).

Neurosurgical approach if aneurysm detected.

Key Clinical Concept – “Light Interval”

Seen especially with epidural hematoma:

LOC at trauma → lucid interval → deterioration with brainstem signs → coma.

Overall Management Principles

1.Emergency: StabilizeABCs, resuscitation.

2.ICPcontrol: Mannitol, hypertonic saline, head elevation.

3.Definitive: Prompt neurosurgical evacuation of hematoma (epidural, subdural, large intracerebral).

4.Supportive: Sedation, anticonvulsants, maintain perfusion & oxygenation.

5.Long-term rehabilitation after surgery (speech, physiotherapy, occupational therapy).

Takeaway:

Compression = mass effect + midline shift → herniation.

Epidural = arterial, lucid interval (classic).

Subdural = venous, acute–chronic.

Treatment is mostly surgical, except very small/chronic lesions where conservative care is possible.

47.Epileptic seizures, definition, classification. Focal points and generalized seizures. Epileptic Seizures

Definition

Epileptic seizure = paroxysmal, stereotyped clinical event caused by excessive, hypersynchronous discharge of neurons in the cerebral cortex.

They can be focal (localized cortical discharge) or generalized (whole brain involvement).

Etiological (Pathogenetic) Classification (Shanko)

1.Epileptic (idiopathic / genetic epilepsy)

2.Anoxic (hypoxia-ischemia related)

3.Toxic-metabolic (hypoglycemia, hypocalcemia, uremia, drugs, alcohol withdrawal)

4.Psychogenic seizures (non-epileptic attack disorder)

5.Hypnotic (sleep-related)

6.Focal seizures (structural brain lesion, e.g., tumor, trauma, scar, cortical dysplasia)

7.Generalized seizures (primary generalized epilepsy syndromes)

8.Undetermined genesis

Clinical Classification (by ILAE, simplified for exams)

A. Generalized Seizures

(Both hemispheres from the start; loss of consciousness always present)

1.Tonic-clonic (Grand mal)

Most common generalized seizure.

Sudden LOC, tonic phase (10–20 sec): tonicity, fall, cry, cyanosis → clonic phase: rhythmic jerks (30–60 sec), postictal confusion.

2.Absence seizures (Petit mal)

Sudden brief LOC (few seconds).

“Freezing,” blank stare, automatisms. No aura, no postictal confusion. Typical in children.