Brain injury😶‍🌫️

Skull Vault Fractures:

Fissure fracture (Linear crack):

• Most common type of skull fracture.

• Caused due to weapon with broad striking surface.

Depressed fracture:

• Caused due to weapon with smaller striking surface (Hammer).

• Also known as signature fracture
• Weapon can be identified

Pond fracture / Ping-pong fracture:

• Variant of depressed fracture.

• Also known as indented fracture/ping pong fracture.

• Seen in infants (Elastic bones) born out of obstetric delivery.

Gutter fracture:

• Associated with oblique bullet/glancing bullet.

Comminuted fracture:

• Multiple fractured segments due to multiple blows to the skull.

• Mnemonic: Communists adich adich kollum

Diastatic fracture:

• AKA sutural fractures

• Fracture line is along the sutures of the skull.

• Seen in young adults.

• Mnemonic: Static → anagatha aal → young adults → fracture also anangilla → along suture lines

Skull Base Fractures:

Ring fracture:

• Characteristics:
• Fracture in base of skull
• Around foramen magnum
• Size: 3-5 cm
• Fracture in posterior cranial fossa.

• Types
1. Fall from height:
• Lands on feet:
• Impact: Legs → Vertebral column → Base of skull
• Lands on buttock:
• Impact: Indirect force to base of skull.
2. Heavy weight on the head.

Hinge fracture/Motorcyclist fracture:

• Type 1:
• Sideway impact in middle cranial fossa.
• Fracture lines reach opposite side
• Through sella turcica & middle cranial fossa

Puppe’s Rule

• The new fracture line will never cross previous fracture line.

• Sequencing the fracture lines due to blows.

Coup & Contrecoup Injuries

• Coup: Injury at site of impact.

• Contrecoup: Injury opposite to site of impact OR Contralateral surface of Ipsilateral lobe.

• Most common site: Occipital impact – Frontal lobe contusion.

• NOTE: Frontal injury
• Will not produce Occipital countercoup

Features

• Occurs in the circle of Willis

Important

• M/c site: 
• Junction of Anterior communicating artery with ACA
• Compresses optic chiasma.

• Most common cranial nerve involved in unruptured or ruptured
• 3rd cranial nerve → ptosis

• M/c location of unruptured that results in 3rd nerve palsy:
• Posterior communicating artery
• Compresses oculomotor nerve

• Rupture leads to subarachnoid hemorrhage (SAH)

• Layer of blood vessel affected in patient
• Internal elastic lamina.

• Most common site of rupture
• If size is >8 mm
• Top of basilar artery.
• At origin of posterior cerebral artery
• Near origin of posterior communicating artery
• M/c rupture: 
• Apex of aneurysm

• Rarest location
• Vertebral artery.

• Rupture of the saccular aneurysm:
• Leads to subarachnoid hemorrhage.

Subarachnoid Hemorrhage (SAH):

Causes

• Most common cause of subarachnoid hemorrhage is
• Trauma >>
• rupture of berry aneurysm/
• mycotic aneurysm/
• staphylococcus aureus.
• complication of Infective Endocarditis.
• rupture of Charcot Bouchard aneurysm.
• due to Hypertension

Clinical Manifestation

• Thunderclap headache/worst headache of life.

• As blood will spill into meninges it will cause nuchal rigidity.

• Source of Bleed:
• Arteries in Circle of Willis.

• Presents with Thunderclap headache.

• Autopsy Findings: Hemorrhage remains intact after pouring water.

Diagnosis: 

• NCCT
• Spillage of blood in Basal cistern (star appearance).
• Star of Death: whiteness in the sylvian fissure from MCA
• Sylvian fissure → separates temporal and parietal lobes.

• SAH can be seen in interhemispheric fissure.

• Investigation shown is DSA
• Black vessel.

• Tortuous artery seen is Internal carotid artery.
• Divides into middle and anterior cerebral arteries.

• Blob of contrast indicates Aneurysm.
• Rupture leads to SAH.

NOTE

• TB meningitis
• Basal exudates on NCCT
• Cobweb coagulum seen in CSF

• If not available, lower ICP with mannitol and do LP (see bloody CSF).
• LP (avoided if raised ICP)
• Bloody CSF may occur.
• LP after 24–48 hr:
• CSF becomes xanthochromic as RBCs break down.
• Also seen in
• Trauma,
• HSV 1 encephalitis
• subarachnoid hemorrhage

• Elevated BNP
• causes natriuresis → decrease in sodium levels of the body → < 125 meq → seizures

• ECG findings:
• MI due to pain and catecholamines
• ST depression and T wave inversion.

Management: 

• NO SURGERY

• With strict complete bed rest advised.

• Platinum endovascular Coiling > Aneurysmal clip
• Angiography → Intervention (coiling/surgical clipping)

Post-op:

• CCBs (Nimodipine) to prevent vasospasm

Xanthochromic CSF

Causes of Death

• Vasospasm leading to cerebral infarction (most common cause of death).
• When the berry ruptures → the blood vessels in the surrounding area → protective spasm → acts as a double insult → causes cerebral infarction.
• Give Nimodipine to prevent vasospasm

• Rebleeding (rebleeding can occur from the same or different site).

• Hydrocephalus.

• Seizures: when Na <125 meq.

• MI

WFNS and HUNT AND HESS Scale for SAH

• Hunt and Hess
• Mild headache
• Moderate headache
• Confusion
• Stupor
• Coma

MR Angiography

• Visualizes brain circulation.

• 35-45% die by 1 month due to complications.

• More incidence in Asians and Blacks.

Causes

• Hypertension.

• Coagulopathy.
• Warfarin toxicity:
• Antidote: Prothrombin complex concentrate >> vitamin k.
• Dabigatran toxicity
• Antidote: IDARUCIZUMAB.
• Mnemonic: Dab → Idaru dab cheyyunnnaaaa
• Apixaban toxicity
• Antidote: Andexanet alpha.

• Cocaine and methamphetamine:
• vasoconstriction in cerebral blood vessels
• → increased pressure and rupture.

• Cerebral amyloid angiopathy
• apolipoprotein E gene: E4, E2
• there occurs weakening of blood vessels in the brain.
• Cause of intracerebral hemorrhage in non-diabetic and non-hypertensive patient.

• Head injury IOC: NCCT (Non Contrast CT).
• NCCT looks for:
• Acute hemorrhage.
• Fracture.

• Exception:
• Diffuse Axonal Injury (uses SW-MRI).

• Decompression craniectomy >> Burr hole / craniotomy

Tension pneumocephalus

• Mount Fuji sign is seen.

• Causes
• Head trauma (most common)
• Post-neurosurgery
• Sinus fractures (frontal, ethmoid)
• CSF leak (skull base defects)
• Infections with gas-forming organisms (rare)
• Positive pressure ventilation
• Barotrauma

Diffuse Axonal injury

• Cause: 
• High-velocity impact,
• shearing force (grey/white matter junction)

• Features: 
• History of RTA, GCS worsening, normal CT.
• Persistent coma (GCS not improving)

• Imaging (IOC): 
• MRI
• Multiple petechial hemorrhages at grey/white matter junction
• Corpus callosum, brainstem areas can be involved.

• Worst prognosis

Adam’s classification of DAI

• DAI has low GCS (aDAM aDAI)
• 1 → Grey mater - white mater jn
• 2 → Corpus callosum
• 3 → Brain stem

Concussion

• Mildest primary brain injury

• Management:
• Avoid contact sports briefly
• No surgical intervention

Secondary Injury: 

• Due to ↑↑ intracranial pressure (ICP)

Cerebral Perfusion Pressure (CPP):

• CPP = MAP - ICP

• Normal: >60 mmHg

• Cushing’s Reflex (due to trauma, increased ICP):
• ↑↑ Mean Arterial Pressure (MAP)
• ↓↓ Heart Rate (bradycardia)
• Altered respiration

• Irregularly irregular breathing (Biot's breathing)
• Irregular pattern
• due to raised ICP.

• hyperpnoea interrupted by sudden apnoea.

• indicates a bad prognosis.

• Seen in:
• Damage to medulla
• meningitis

• Mnemonic: Bite (Biots) Me (Meningitis, Medulla)

• 2 changes → Bi Ots

Target: ICP<20mm and CPP >60mm

1. Elevate head end

2. Ventriculostomy

3. Mannitol

4. Steroid
• Use in tumor, abscess
• CI in head trauma / stroke/ hemorrhage

5. Hyperventilation

6. Vasopressors

Management of Increased ICP

• Adequate O2 saturation

• Adequate perfusion (SBP >100 mmHg)

• Avoid hyperglycemia (increases cerebral edema)

• Administer IV mannitol

• Moderate hyperventilation

• Seizure Prophylaxis (Phenytoin/Valproate):
• Useful for early PTS
• Not recommended for late post-traumatic seizures (PTS)

• NOs in Head Trauma
• No steroids in head trauma
• Hypotonic solutions
• Dextrose solutions
• Both promote cerebral edema

Goals of Rx

• ICP: 20–25 mmHg

• CPP: ≥ 60 mmHg

• Na⁺: 135–145

• SBP: ≥ 100 mmHg

• MAP: >90

Glasgow Outcome Score

• Prognostic score after head injury

• Score & Prognosis:
• 1: Death
• 2: Persistent vegetative state
• 3: Severe disability (conscious)
• 4: Moderate disability
• 5: Good recovery + mild disability

Raised ICT

Intraparenchymal Hemorrhage / Contusion:

• Most common type

• Management: Conservative (manage increased ICP)

• Acute hemorrhage is white (Hyperdense).

• Most common cause: HTN.

• Most common site: Putamen (basal ganglia).

• Charcot’s Artery bleed
• Lenticulostriate branches Of MCA rupture first.

Hypertensive Intracerebral Hemorrhage

• M/c site of bleed is putamen

• If cerebellar hamartoma is > 3cm
• obstructive hydrocephalus
• requiring a surgical intervention.

Clinical Features

• Develop over 30-90 minutes after the bleed.

• Contralateral sagging of face.

• Slurring of speech.

• Arm weakness.

• Eye deviation
• In a cortical stroke
• eyes deviate towards the side of the stroke.
• In sub cortical stroke
• eye looks away from the stroke.

• Irregularly irregular breathing (Biot's breathing) due to raised ICP.
• indicates a bad prognosis.

• Decerebrate posturing/Rigidity.

• Coma.

Thalamic Haemorrhage

• Contralateral hemiplegia, hemianesthesia.

• Chronic debilitating contralateral pain (Dejerine Roussy syndrome).
• Severe pain → Acid over half of body → when water falls on body

Pontine Hemorrhage

• Deep coma.

• Quadriplegia.

• Hypertension,

• Pinpoint pupil (~1 mm) + ↑↑ respiratory rate
• Key diff between Pontine hemorrhage and Drug overdose

• Hyperhidrosis

• Hyperthermia

Cerebellar Hematoma

• Occipital headache.

• Vomiting.

• Ataxia.

• Hematoma > 3 cm
• needs a neurosurgical intervention

Posterior Reversible Leukoencephalopathy

• Patient is a known case of hypertension with features of raised ICP.
• Cause of hypertension could be any;
• acute glomerulonephritis,
• CKD,
• toxemia of pregnancy.

Clinical Presentation

• Headache.

• Vomiting.

• Retinal hemorrhage on fundus examination.

• Convulsions

• Stupor and coma.

MRI Head Shows

• Vasogenic cerebral oedema in occipital region.

Treatment

• Reduce blood pressure.

Extradural Hemorrhage (EDH):

• Young patient

• Type of coup injury
• High-velocity impact

• Fracture of temporal bone Pterion
• meeting point of 4 bones:

• Frontal bone

• Parietal bone

• Greater wing of sphenoid

• Squamous part of temporal bone

• Rupture of middle meningeal artery
• Anterior division

• Bleed in the extradural space.

• Brainstem compression.

• Death due to respiratory failure.

• Features: 
• Lucid interval (Period of unconsciousness b/w 2 periods of consciousness)

• Imaging:
• Biconvex opacity
• Restricted by sutures
• Swirl sign:
• Hypodense area + Hyperdense area ⇒ S/O active hemorrhage.
• Needs Decompression
• Acute hemorrhage
• hyperdense on CT.

• Management: Decompressive > Burr hole / craniotomy close to pterion

• Autopsy Findings: Clearing of hemorrhage after pouring water.

Structures Lying Deep to Pterion

• MMA

• Middle cerebral vessels

• Sylvian fissure/ lateral sulcus
  → sulcus between frontal and temporal lobe

• Insula

• Broca’s area

• Lesser wing of sphenoid

Lucid Interval

• Period of consciousness between 2 periods of unconsciousness.

• Seen in EDH > SDH.

• Medicolegal importance:
• Patient can provide valid evidence, will & is criminally liable.
• Death due to failure in diagnosing lucid interval:
• Medical negligence.
• Punishable under 106(1) BNS.
• Mnemonic: Lucy ye 106 idi idich konnu

Subdural Hemorrhage (SDH):

• Trivial injury

• Elderly patient

• Superior cerebral vein (Bridging vein)

Risk factor: Mnemonic ABC.

• Aged person with minor trauma.

• Boxers → c/c sdh

• Child abuse (Shaken baby syndrome).

Features: 

• Gradual altered sensorium after few weeks

Types:

• Acute: Within hours of injury

• Subacute: Hours to days post-injury

• Chronic: Days to weeks post-injury

• Source of Bleed: cortical bridging veins/dural venous sinuses.

• Imaging: Crescentic opacity.
• Not restricted by sutures

Management:

• Decompression craniectomy >> Burr hole / craniotomy

• Indications for Craniotomy (SDH): (any 1)
• Clot size >30 cc
• Midline shift >5 mm
• Clot thickness >1.5 cm

• Autopsy Findings:
• Clearing of hemorrhage after pouring water.

Note

Plaque jaune lesions

• Type of traumatic brain injury

• Due to multiple concussions (Boxing)

• Features
• Depressed
• Retracted
• Yellowish-brown

• Contrecoup areas

Hematoma

Management of Intracerebral Hemorrhage

ICH Score
(Mnemonic: AHIIG)

• A - Age.

• H - Hematoma volume.
• > 3cm

• I -
• Infratentorial location of bleed
• Located in 4th ventricle
• high chances of developing obstructive hydrocephalus
• worse prognosis as compared to supratentorial bleed.

• I -
• Intraventricular hemorrhage
• In Neonates
• common after birth trauma
• e.g. faulty forceps delivery.
• Shrill cry.
• Bulging anterior fontanelle.
• Pallor.
• IOC
• USG done to evaluate, NOT CT
• In adults
• Due to extension from Intracerebral bleed

• G - GCS.

Specific Management of ICH

• Airway protection - with intubation.

• BP control:
• NICARDIPINE >> sodium nitroprusside is used.
• Sometimes nicardipine can cause reflex tachycardia.
• ESMOLOL is used to neutralize in such patients.
• Target blood pressure is < 140 mmHg (page 3349 Harrison).

• Treatment of coagulopathy.

• Midline shift/obtundation in patient
1. osmotic diuretics are used.
• 3% Mannitol
• 5% dextrose is NEVER USED in management.
2. If Mannitol fails, we can perform:
• VENTRICULOSTOMY
• A drain is placed in the lateral horn of the ventricle.
3. If the pressure is still rising,
• then neurosurgical decompression has to be done based on the ICH score.

DWI (Diffusion Weighted Imaging)

• Most sensitive for Acute Stroke.
• Acute infarct shows restricted diffusion.

• ADC (Apparent diffusion coefficient)
• Based on Brownian movement of protons.
• Protons move freely like CSF (Facilitated diffusion).
• Brown (Brownian movement) people diffuse (Diffusion weighted MRI) into other areas very easily

• NOTE: MRI → Gyroscopic movement of protons

Diffusion restriction

• Normal fluid diffuses

• Fluid does not diffuse when Na K pump not working (d/t Ischemia), Eg
• Ischemic Stroke
• Epidermoid cyst (d/t thick secretions)
• CSF-like mass
• Abcess (thick pus)
• Hypercellular tumor

• Note:
• Arachnoid Cyst
• Doesnt show diffusion restriction
• shows FLAIR suppression
• Ara → Arum allathavan → has no flair → but go everywhere (no diffusion restriction)

SWI (Susceptibility Weighted Imaging)

• Identifies MicroHemorrhages and Calcification.

• They appear as black areas of blooming

• IOC: DAI

• Mnemonic: Susceptible people bloom → when beaten down (hemorrhage)

MR Tractography/ DTI (Diffusion Tensor Imaging)

• Done for white matter tracts

• Based on anisotropy of white matter tracts

• Tractor (MR Tractography) operation → Tension (DTI) for white people (white matter)

BOLD MRI / FMRI (Functional MRI)

• Locates functional/eloquent areas of the brain.
• Visual cortex.
• Speech area.
• Auditory cortex.

• Helps in neurosurgery planning.

• Mnemonic: Bold () people are functional () → they can see, hear and speak well () → plan to become Neurosurgeons ()

Brain Death:

• Certification: Requires 2 expert physicians

• Criteria to Declare Brain Death:
• GCS = 3
• Non-reactive pupils
• Absent brainstem reflexes
• No spontaneous ventilatory effort
• Positive apnea test
• Preoxygenate with 100% O2 → Extubate
• When pCo2 >60mm → if No spontaneous effort
• Absence of confounding factors
• e.g., alcohol, drug intoxication, hypothermia

• Definition:
• Irreversible cessation of all functions of the entire brain
• including the brain stem.

• Brain Death in children is usually due to trauma or asphyxial brain injury.

Diagnosis of Brain death:

• 3 Key Components:
1. Irreversible coma with a known cause.
2. Apnea:
• Absence of respiratory efforts
• adequate stimulus (PCO2 >60 mm Hg).
3. Absence of brain stem reflexes
• light reflex,
• corneal reflex,
• gag reflex

• All must remain consistent for
• 2 observations
• observation period of 24 hrs - 48hrs.

Features incompatible with the diagnosis of brain death:

• Decerebrate/Decorticate posturing.

• Presence of seizures.

• Extensor or flexor response to painful stimulus.

NOTE:

• Loss of DTR and Loss of stretch reflex is not needed for diagnosis of brain death

Layers of Scalp

1. Skin

• Thick

• Connected to aponeurotic by connective tissue

• Content: Hair, sebaceous, and sweat glands

2. Connective Tissue

• Blood vessel walls tightly adherent to stroma

• Lacerations bleed heavily (cannot vasoconstrict)

• Applied aspect: Injury → Profuse bleeding

3. Aponeurotic Layer

• Galea Aponeurotica

• Content:
• Frontal belly (of occipitofrontalis)
• Occipital belly

Surgical layer:

• Skin + Connective Tissue + Aponeurotic Layer (Galea Aponeurotica)

• Easy plane of cleavage

• Tissue expanders/implants are placed under this layer

• Subaponeurotic bleeding → "Black eye"

4. Loose Areolar Tissue (Danger Area of Scalp)

• Retrograde infection via emissary veins
• Emissary veins (valveless) → Scalp veins ⇔ Dural venous sinuses → Cavernous sinus thrombosis

• Bidirectional flow:
• → If intracranial pressure ↑
• ← If intracranial pressure ↓

• Applied aspect:
1. Infection of scalp spreads to Dural venous sinuses
2. Injury
• Blood doesn't move posteriorly/laterally (bony origin of occipital belly)
• Collects under loose areolar layer
• Gravitates anteriorly (frontal belly) → Black eye

5. Pericranium

• Periosteum

• Loosely arranged (except at sutures)

NOTE: β 2

• Microglobulin → Multiple Myeloma, Dialysis

• Transferrin → CSF

• Glyocoprotein → APLA