Intracranial Trauma

(Traumatic brain injury TBI). Glascow coma scale (GCS) 13-15 is mild, 9-12 moderate, </=8 severe head injury; outcome dependent on type of injury. Initial GCS correlates with immediate morbidity and mortality, but is unreliable for predicting long-term outcome (as with CT findings).

  • Eye opening – 4 spontaneous; 3 to voice; 2 to pain; 1 none.
  • Best verbal – 5 oriented; 4 confused; 3 inappropriate words; 2 incomprehensible words; 1 none.
  • Best motor – 6 obeys; 5 localises; 4 withdraws; 3 abnormal flexion; 2 extension posture; 1 flaccid.

Number of DAI lesions and brainstem/corpus callosum involvement associated with low GCS and poor long-term prognosis. Cortical contusions and epidural/subdural haematoma don’t correlate with long-term outcome unless there is significant mass effect. Higher chance of positive CT if there is HA, vomiting, >60yo, intoxication, short term memory deficit, physical evidence of trauma above the clavicles, coagulopathy, seizure.

Primary Head Injury

From direct result of trauma including skull fractures, parenchymal and/or vascular injuries. Injury may be from inertial injury/rotational acceleration (most injuries, don’t require direct impact -> DAI, shearing SDH); or parenchymal compression and rarefaction in direct impact with skull (coup and contrecoup). Contusions and haematomas are more severe with very short periods of acceleration/deceleration (eg falls); DAI and gliding contusions are associated with longer acceleration/deceleration times (eg MVA). Haematomas may be iso/hypo-dense in severe anaemia, DIC or hyperacute active bleeding (also causes fluid-fluid levels, sedimentation).

Concussion

Transient impairment of neurologic function, may be associated with LOC at time of injury. ?Dysregulation of reticular activating system. Post-concussion syndrome (cognitive deficits from TBI) includes reduced processing speed, poor attention/concentration/memory, impaired reasoning/language/constructional skills. Controversial correlation with degree of injury. Higher risk of Alzheimer disease, loss of brain parenchyma (caudate nucleus, corpus callosum, hippocampus, fornix, thalamus). Post-traumatic thalamic atrophy from cortical and subcortical lesions ?transneuronal degeneration. Hyertrophic olivary degeneration from injuries to red nucleus, dentate nucleus, central tegmental tract, cerebellar peduncles. Wallerian degeneration of corticospinal tract after motor area contusions/shears. A cavum septum pellucidum may develop from repetitive head trauma tearing septal walls.

Skull Fractures

May be linear (little clinical significance), diastatic, comminuted or depressed. Surgery is indicated for depressed or compound fractures. Depressed fractures are associated with underlying contusion. Pneumocephalus from compound fracture or invovement of sinuses, hence risk of infection.

Temporal bone fractures – Deafness, facial nerve palsy, vertigo, dizziness, nystagmus, haemotympanum, CSF otorrhoea, ecchymosis over mastoid process (‘Battle’s sign’). Opacification of mastoid air cells, fluid in middle ear cavity, pneumocephalus, pneumolabrynth, dislocation or fracture of ossicles. Best seen on thin-section (1-1.5mm) axial and direct coronal CT. Fracture type depends on alignment to long axis of the petrous bone.

  • Longitudinal – Blow to side, highly associated with temporal lobe injury.
  • Transverse – Blow to occiput/frontal region, more severe, facial palsy in 30-50%, may involve carotid canal or jugular foramen.
  • Mixed – Severe crushing blow.

Scalp Haematoma

Subgaleal haematomas between galea aponeurosis and pericranium. Can be very large, can cross sutures.

Cephalomaematoma lie between the pericranium (periostium) and skull bone. Usually small, more focal, confined by the suture.

Extradural Haematoma (EDH)

(Epidural haematoma). 90% arterial, from skull fracture (in 85-95%) disrupting middle meningeal artery, may be without fracture esp children (greater elasticity of skull). In 50% neurologic deterioration occurs after a lucid interval (cf DAI immediately). Haematoma strips dura from inner table skull. Most temporal/temporoparietal. Venous epidural is less common, from disrupted dural venous sinus, tends to be at vertex, posterior fossa, anterior middle cranial fossa. Dense, lenticular/biconvex, mass effect, usually don’t cross cranial sutures (periosteal layer firmly attached) apart from vertex (outer wall sagittal sinus is less adherent). Occasionally heterogeneous where hypodensity may be active extravasation, unclotted blood or serum excluded from clot. Occacional fistula between meningeal arteries/veins or pseudoaneurysm.

Venous EDH:

  • Superior sagittal sinus at vertex, transverse sinus futher laterally. Because they are located between the dural sleeves they can cross sutures. Vertex and transverse sinus EDH can enlarge slowly.
  • Anterior middle cranial fossa are small self-limited, always associated with a fracture. Limited medially by sphenoorbital fissure and laterally my sphenotemporal suture.
  • Clival venous plexus – along posterior surface clivus. Usually small, self limited.

Subdural Haematoma (SDH)

Usually venous from stretching/tearing of bridging cortical veins traversing subdural space to dural sinuses; may be injury to penetrating branches of superficial cerebral arteries. Acute decceleration of MVA or fall, or penetrating injury. Increased risk in elderly (increased CSF spaces hence longer stretched out bridging veins) and infants (thinner-walled bridging veins). Usually present within 48hrs with slowly progressive headache and confusion, 10% bilateral. Simple if no parenchymal injury, complicated where parenchymal injury is usually more clinically significant. Diffuse swelling of underlying hemisphere common, from excitotoxic brain injury causing more mass effect than expectedb, can get very severe. Burst lobe – intra-axial blood continuous with SDH. Dense, cresenteric axially but frequently lentiform/biconvex coronally, most supratentorial, frequently along falx and tentorium, inwardly displaced cortical vessels. Do not cross dural reflections. Small SDH masked by blooming of adjacent bone, hence need for intermediate/subdural window. Tentorial SDH between leaves of tentorium, fades out laterally and stops at medial margin. Acute haematoma is hyperdense retracted clot (50-60HU), progressively reducing with lysis and protein degradation, isodense at 1-3/52. Acute blood may be isodense/hypodense in severe anaemia, extravasation (hyperacute) or tear in arachnoid membrane allowing CSF dilution. Sentinal clot – swirling, sign than the haematoma will increase in size. Acute blood shows diffusion restriction. Fibroblasts from dural surface grow into the haematoma at 2/52, hyalinised connective tissue at 1-3/12, retracting to dural surface leaving a thin layer of reactive connective tissue (subdural membrane). Rebleeding (coagulopathy, alcoholism, age, epilepsy, ventricular shunt surgery; highest risk in first few months) causes heterogeneity, sediment level (haematocrit effect, also seen with clotting disorders), fibrous septations and loculations. Chronic SDH (most >50yo, also in birth trauma, vitamin K deficiency, coagulopathy, child abuse) are hypodense similar to CSF, may become convex, may rarely ossify or contain fat. If contrast is given subdural membranes enhance after 1-3/52. In elderly SDH usually larger due to generalised parenchymal loss allowing unimpeded haematoma growth before mass effect and symptoms.

Subdural Hygroma

Subdural fluid collection with similar characteristics or slightly higher protein than CSF. From acute tearing of arachnoid membrane. Most common <10yo and >10yo. Can get haematohygroma with combined with bleed. Also seen after vetriculostomy, ventricular decompression, H.influenzae meningitis, marsupialisation of arachnoid cyst, intracranial hypotension. Acute growth may cause mass effect. Displaces cortical veins (lie just under arachnoid membrane) inwards against brain surface (traverse through fluid in atrophy), hence suspect if cannot see vessels in fluid. May be high on FLAIR (protein) or have susceptibility. DDx benign macrocephaly of childhood (dilated subarachnoid space and veins crossing in fluid), arachnoid cysts (may be traumatic, may remodel bone or have mass effect cf hygromas, also displaces vessels inwards).

Spontaneous intracranial hypotension may cause postural headache, from dural tears and CSF leakage eg after lumbar puncture. Leak point may be seen on CT myelography, radionuclide cisternography, high-resolution MR. May see bilateral subdural hygromas, tonsillar descent, brain stem sagging, enlarged pituitary gland, pachymeningeal enhancement, subcortical white matter reduced FLAIR, enlarged spinal venous plexus, nerve root sleeve thickening. Tx post-LP is epidural blood patch.

Traumatic Subarachnoid Haemorrhage

Common, but rarely large enough to cause significant mass effect. Disruption of small subaracnoid vessels or direct extension from contusion or haematoma. Linear density within cisterns and sulci causing apparent effacement. Hyperacute blood best seen on FLAIR; CT better than T1WI and T2WI. Chronic haemorrhage causes haemosiderin staining (superficial haemosiderosis) with marked reduction in T1 and T2 signal. May cause subsequent hydrocephalus by imparing CSF resorption at arachnoid villi. DDx apparant hypderdense vessels on a background of cerebral oedema.

Intraventricular Haemorrhage (IVH)

From rotational tearing of subependymal veins on surface of ventricles, direct extension of parenchymal haematoma, or retrograde flow of SAH via 4th ventricle. Risk of obstructive hydrocephalus at level of aqueduct or arachnodi villi. Hyperdense dependent layering in ventricles esp occipital horns.

Cerebral Contusion

Focal bruising and petechial haemorrhages; haemorrhage may extend into white matter and rarely into SAH/SDH. Common in severe trauma. Crests of gyri most susceptible, usually near bony protuberances, multiple and bilateral. Common at temporal lobes above petrous bone or posterior to greater sphenoid wing, frontal lobes above cribriform plate and along orbital ridges, planum sphenoidale and lesser sphenoid wing, along falx/tentorium, at margins of depressed fractures (direct trauma), <10% involve cerebellum. Coup contusion at site of impact, contrecoup diametrically opposed, intermediate-coup at deeper structres of brain. Gliding contusions along superior parasagittal hemispheres esp frontal lobes. Nonhaemorrhagic lesions are initially poorly seen, more obvious in 1st week from oedema. Haemorrhagic lesions (more common than DAI) are hyperdense with surrounding oedema. May be wedge-shaped, involve crowns of gyri. Central haematoma is surrounded by penumbra (damaged tissues with endothelium prone to rupture with time), parapenumbra. ‘Salt and pepper’ pattern – mixed areas of hypodensity and hyperdensity (best seen in subacute phase). MR poorly-defined high PD/T2 in gyral pattern, haemosiderin staining. May develop blood-fluid levels with haemorrhage into contused necrotic brain or coagulation defects. Tx surgical decompression. Chronic -> focal encephalomalacia, plaque jaune (retracted yellow-brown patches).

If given contrast, this may leak into damaged tissues surrounding the intra-axial haematoma (penumbra), mimiking enlargement of haematoma on subsequent C- CT. This may be differentiated on virtual non-contrast DECT. This enhancing penumbra is prone to haematoma expansion.

Intracerebral Haematoma

Shear-induced haemorhage from rupture of intraparencymal vessels. Less oedema than cortical contusions. Most in frontotemporal white matter, occasionally in basal ganglia. Often associated with fracture and other brain injury. May be lucid before mass effect with expanding haematoma, may present late from delayed haemorrhage.

Diffuse Axonal Injury (DAI)

Widespread disruption of axons (complete or incomplete disruption) during rapid acceleration or deceleration (mostly MVA), may be distant from site of direct impact. Disruptions occur at the nodes of Ranvier (myelin sheath gaps). LOC/coma typically starts immediately or shortly after trauma (50% of patients with this have DAI). Within days axonal swelling (retraction ball) develops, in weeks microglial clusters, months Wallerian degeneration. Best seen on DWI and diffusion tensor imaging with 3D tractography. Can get associated diffuse vascular injury (DVI) with small petechial haemorrhages (usually complete axonal disruption) with surrounding oedema; on MR low T2/high T1 within a few days, periarterial/perivenous extending along penetrating vessels, best seen on susceptibility imaging. Nonhaemorhagic areas (80%) are multiple (15-20) oval ill-defined hypodensities with long axis parallel to fibre bundle direction, small foci of increased T2, subtly reduced T1 within white matter. Residual findings include nonsepcific atrophy, haemosiderin staining (may persist for years). Mild form confined to frontal (parasagittal) and temporal (periventricular) white matter near grey-white junction; more severe also involves corpus callosum (esp posterior body and splenium, due to thicker falx posteriorly preventing cerebral hemisphere from crossing; seen in 20% of all DAI, may cause IVH); most severe involves dorsolateral quadrant of rostral midbrain and upper pons (esp medial lemnisci and cerebellar peduncles), internal capsule and subcortical white matter. May disrupt septum pellucidum and ventricular blood supply due to disruption of subependymal veins/capillaries.

  • Pontomedullary separation/rent – Rare axonal injury variant from severe lateral or hyperextension injury eg MVA vs pedestrian. Tear in ventral pontomedullary junction or cerebral peduncles. May be small tear to complete avulsion. Usually fatal. Associated with petrous bone fractures, fracture-dislocations of cervical spine, ring fractures of foramen magnum.

Penetrating Injuries

From bullets, stabs or bone fragments. May cause dissection, acute haemorrhage, pseudoaneurysm with delayed haemorrhage. Pneumocephalus implies communication with extracranial space eg sinus, may rarely develop into pneumatocoele where gas is trapped and expands in brain via ball-valve mechanism. Tension pneumocephalus indents the brain, may cause Mount Fuji sign at the anterior frontal lobes separating the interhemispheric fissure. Brain may adhere to dura via fibroglial scar, later causing seizures.

Subcortical Grey Matter Injury

Uncommon. Multiple petechial haemorrhages usually basal ganglia and thalamus, periaqueductal rostral brainstem (poor progmosis) from microscopic perivascular bleeds of disrupted small perforating vessels.

Vascular Injuries

Includes dissection, occlusion, pseudoaneurysm, AV fistula (CCF or dural fistula from middle meningeal aa and vv). Associated with base of skull fractures. Most common ICA injury at sites of fixation (esp midway between cavernous and bifurcation, entrance to carotid canal at base of petrous, exit from cavernous sinus below anterior clinoid process). May be associated with parenchymal infarct. May cause SAH with very high mortality.

Carotico-Cavernous Fistula (CCF)

Injury to cavernous ICA causing direct fistula to surrounding venous plexus. Associated with severe injury, skull base fracture esp sphenoid, may be from ruptured cavernous carotid aneurysm. Venous engorgement of cavernous sinus and tributaries (superior ophthalmic vein, inferior petrosal sinus, veins around foramen ovale, middle cerebral veins), proptosis, swelling of preseptal soft tissues, enlarged extraocular muscles, findings may be bilateral (interconnecting venous channels). Confirmed with carotid angiography demonstrating site of fistula. Drainage through cortical veins is prone to intraparenchymal haemorrhage. May also cause SAH, intraorbital haemorrhage, epistaxis, otorrhagia, glaucoma, dilated conjunctival vessels, ophthalmoplegia, raised ICP.

Secondary Head Injury

Consequence of primary injury, usually from mass effect or vascular compromise. Often preventable. Includes cerebral swelling, brain herniation, hydrocephalus, ischaemia, infarction, CSF leak, leptomeningeal cyst, encephalomalacia, infection. Prognosis is worse with reduced NAA, effacement of mesencephalic cistern, SAH, acute SDH, DAI, positive DWI, perfusion deficits/ischaemia. Elevated ICP occurs in 10-15% of severe head injury with normal scan. Increased risk of post-traumatic epilepsy, meningioma, infectious diseases, psychiatric disorders.

Diffuse Cerebral Swelling

Effacement of sulci, suprasellar and quadrigeminal plate cisterns, compression of ventricles. May be from:

  • Hyperaemia – Increased cerebral blood volume, ?loss of normal cerebral autoregulation. Most common in children/adolescents.
  • Cerebral oedema – Release of excitatory neurochemicals glutamate and aspartate causing intracellular Ca and Mg, free radicles, cytokines, proteases, neuronal death, cytotoxic and vasogenic oedema. Reduced attenuation with loss of grey-white differentiation. Cerebellum and brainstem usually spared, may appear relatively hyperdense. Falx and cerebral vessels may appear dense mimicking SAH. In acute setting cytotoxic swelling is a major cause, positive on DWI.

Herniation Syndromes

May be from mass effect in trauma, intracranial haemorrhage, infarction or neoplasm.

  • Subfalcine/cingulate herniation – Most common, cingulate gyrus displaced across mildline under falx. Compression of adjacent ipsilateral lateral ventricle, enlarged contralateral ventricle from obstructed foramen of Monro. Both ACAs may lie on same side, at risk of ACA infarction in callosomarginal branch distribution (trapped againsed falx). May also compress internal cerebral veins. Midline shift best measured from septum pellucidum at level of foramen of Monro, significant when >/= 3mm. Contralateral CSF space along anterior falx may be widened.
  • Central transtentorial herniation – Descending herniation effaces suprasellar and perimesencephalic cisterns, inferior displacement of the pineal gland (usually same level as calcified coroid plexus in trigones). May compress CNIII, PCA, anterior choroidal aa, midbrain, contralateral cerebral peduncle. Compression of CNIII and contralateral peduncle causes blown pupil and ipsilateral hemiparesis. Elongation of brainstem AP with narrowing in transverse axis. Ipsilateral ambient cistern widening from contralateral temporal lobe dilatation, cisternal obliteration, brainstem rotation/contralateral sliding.
    • Uncal/temporal lobe herniation – Medial temporal lobe displaced medially over free margin of tentorium. Term usually used when transtentorial herniation is less severe and there is less downward force. Focal effacement of ambient cistern and lateral suprasellar cistern.
    • Kernohan(-Woltman)’s notch phenomenon – Contralateral cerebral peduncle pushed againsed the tentorium creating a notch, associated with infarction/haemorrhage.
    • Duret/secondary brainstem haemorrhages – Midline linear/flame shaped haematoma in tegmentum of rostral pons and midbrain asoc with descending transtentorial herniation, usually midline/paramedial. ?From stretching/tearing of penetrating aa with caudal displacement.
  • Upward/ascending transtentorial herniation – Upwards herniation of superior vermis from superior cerebellar mass effect or rapid decompression of supratentorial pressure. Effacement of superior vermian, ambient and quadrigeminal cisterns. Straightening of normal upward smile of quadrigeminal plate cistern. May compress aqueduct causing obstructive hydrocephalus.
  • Tonsillar herniation – Usually posterior fossa haematoma with cerebellar tonsils displaced through foramen magnum. Effacement of cisterna magna. Causes brainstem compression, compromising respiratory and cardiac centres in medulla oblongata.
  • Externial herniation – Through calvarial defect.

Post-Traumatic Hydrocephalus

From SAH or ICH (impaired resorption at arachnoid granulations or obstruction at aqueduct or 4th ventricle outflow), or mass effect compressing aqueduct/4th ventricle outflows directly. Compressed foramen of Monro causes asymmetric lateral ventricle dilatation.

Ischaemia/Infarction

From raised ICP, embolism from dissection, or direct mass effect on vessels from herniation (ACA from subflacine, PCA from uncal, PICA from tonsillar) or extra-axial collection. Diffuse ischaemia from acute reduction in blood flow or hypoxaemia (respiratory arrest, status epilepticus), causing watershed infarcts. Fat emboli from long bone fractures may cause diffuse white matter ischaemia with diffusion restriction, may be worsened with hypoxia due to pulmonary complications.

CSF Leak

Dural tear, associated with fracture. Subarachnoid space communication in CSF rhinorrhoea with paranasal sinuses or middle ear cavity, otorrhoea with middle ear associated with disrupted tympanic membrane. May cause recurrent meningeal irritation. Best seen on radionucline cisternography or CT with intrathecal contrast.

Leptomeningeal Cyst

(‘Growing fracture’). Tear in dura allowing outpouching of arachnoid causing progressive slow widening of skull defect or suture (?from CSF pulsations). More common in children.

Encephalomalacia

Tissue loss with surrounding gliosis. May be asymptomatic or focus for seizure. Well-defined low attenuation with volume loss, ex-vacuo dilatation. Common anteroinferior frontal and temporal lobes. Wallerian degeneration is volume loss along white matter tracts with cell death.

Secondary Brainstem Injury

From downard herniation, hypoxia or ischaemia, usually involving ventrolateral aspect (cf dorsolateral primary lesions).

Post-Traumatic Dementia

(Punch-drunk syndrome, dementia pugilistica). Repeated head trauma over protracted period. Hydrocephalus, thinning of corpus callosum, DAI, neurofibrillary tangles (esp medial temporal lobes), diffuse amyloid β plaques.

Nonaccidental Injury (NAI)

80% of deaths from head trauma <2yo.

  • Depressed fractures, fractures crossing midline, involving occiput.
  • Subdural haematomas of varying ages, usually posterior interhemispheric fissure, convexity, over tentorium, skull base or posterior fossa. SDH of various ages best seen on MR, but note SDH also tend to rebleed spontaneously. DDx benign enlargement of subarachnoid space of infancy.
  • Shaken baby syndrome – Violent shaking causing rotational and shear forces. Retinal and vitreous haemorhages, SDH (esp interhemispheric), SAH, EDH, IVH, contusions, diffuse cerebral swelling, DAI, upper cervical cord haematomas, fractures of skull, vertebrae (compression, fracture-dislocation, spinous process).
  • Diffuse brain swelling ?from vasodilation with loss of autoregulation; from strangulation, smothering, aspiration or other hypoxia. Global effacement of subarachnoid space, compressed ventricles, loss or reversed grey-white matter differentiation, hypodense cerebral hemispheres with relative sparing of brainstem, cerebellum (white cerebellum sign) and deep grey matter. Hypoxic injury pattern I watershed zones; III cortex and basal ganglia diffusely, disrupted blood-ocular barrier with enhancement in globes; II combination of I&III.
  • Sequalae include chronic subdural collection (may calcify), global cerebral atrophy, encephalomalacia.