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Differential Diagnosis of Nervous System Disorders

Diffusely Swollen Hemispheres!!navigator!!

  1. METABOLIC
    1. Metabolic encephalopathy: eg, uremia, Reye syndrome, ketoacidosis
    2. Anoxia: cardiopulmonary arrest, near-drowning, smoke inhalation, ARDS
  2. NEUROVASCULAR
    1. Hypertensive encephalopathy
    2. Superior sagittal sinus thrombosis
    3. Head trauma
    4. Pseudotumor cerebri
  3. INFLAMMATION / INFECTION
    eg, herpes encephalitis, CMV, toxoplasmosis

Brain Edema!!navigator!!

= increase in brain volume ← increased tissue-water content (80% for gray matter + 68% for white matter is normal)

Etiology:

  1. Cytotoxic edema
    reversible increase in intracellular water content 2° to ischemia / anoxia (axonal pallor) → depletion of ATP → ion pump dysfunction across glial cell membrane → increase in intracellular Na+ and K+
    • characteristically seen in cerebral infarction
    • 30–60 min after onset of symptoms
    • decreased ADC value (dark)
  2. Vasogenic edema (most common form)
    fluid leakage of water out of capillaries into extracellular interstitial space ← damage of capillary endothelium; increase in pinocytotic activity with passage of protein across vessel wall into intercellular space
    • associated with primary brain neoplasm, metastases, hemorrhage, inflammation, infarction
    • takes >3–6 hours; requires residual / reestablished blood flow
    • lack of contrast enhancement means breakdown of blood-brain barrier is NOT the cause
    • increased ADC value (bright)

    DDx: blood-brain barrier break-down after 8–10 days

Types:

  1. Hydrostatic edema
    rapid increase / decrease in intracranial pressure
  2. Interstitial edema
    increase in periventricular interstitial spaces ← transependymal flow of CSF with elevated intraventricular pressure
  3. Hypo-osmotic edema
    produced by overhydration from IV fluid / inappropriate secretion of antidiuretic hormone
  4. Congestive brain swelling
    rapid accumulation of extravascular water as a result of head trauma; may become irreversible (brain death) if intracranial pressure equals systolic blood pressure
  • decreased distinction between gray + white matter
  • compressed slitlike lateral ventricles
  • compression of cerebral sulci + perimesencephalic cisterns
    CT:
    • areas of hypodensity
    • Edema is always greatest in white matter!
    • mass effect: flattening of gyri, displacement + deformation of ventricles, midline shift
    • return to normal: from nonhemorrhagic edema / brain atrophy, from white matter shearing injury

    MR:
    • decreased intensity on T1WI
    • increased intensity on T2WI
    • enhancement with gadolinium

    US:
    • generalized / focal increase of parenchymal echogenicity with featureless appearance
    • decreased resistive indices

Midline Cyst!!navigator!!

  1. Cavum septi pellucidi
  2. Cavum vergae
  3. Cavum veli interpositi
  4. Colloid cyst anterior + superior to cavum septi pellucidi
  5. Arachnoid cyst in region of quadrigeminal plate cistern
    • curvilinear margins

Intracranial Nonneoplastic Cyst!!navigator!!

Characteristics:

  • no detectable wall / associated soft-tissue mass
  • homogeneous signal intensity identical to CSF
  • absence of surrounding edema / gliosis
  • NO contrast enhancement
  1. Choroid plexus cyst (most common, abnormal DWI in ⅔)
  2. Ependymal cyst
  3. Neuroglial cyst
  4. Enlarged perivascular spaces (typically multiple, clustered around basal ganglia)
  5. Arachnoid cyst (typically extraaxial)
  6. Porencephalic cyst (communication with lateral ventricle, surrounding gliosis)
  7. Infectious cyst of neurocysticercosis (<1 cm, partially enhancing)
  8. Epidermoid cyst

Cyst with Mural Nodule!!navigator!!

  1. Ependymoma
  2. Pilocytic astrocytoma (childhood)
  3. Pleomorphic xanthoastrocytoma
  4. Ganglioglioma
  5. Glioblastoma multiforme
  6. Hemangioblastoma (posterior fossa, spinal cord)

Multiple Tiny CNS Cysts!!navigator!!

  1. DIFFUSE DEGENERATIVE DISEASE
  2. DIFFUSE INFLAMMATORY PROCESS
  3. LOW-GRADE CYSTIC NEOPLASM
    1. Ganglioglioma
    2. Pyelocytic astrocytoma
    3. Pleomorphic xanthoastrocytoma

Anterior Temporal Cysts with Leukoencephalopathy

  1. Congenital CMV infection
  2. Leukoencephalopathy with subcortical temporal cysts and megalencephaly
  3. Vanishing white matter disease

Cystic Lesions on Head Ultrasound!!navigator!!

  1. NORMAL VARIANTS
    1. Cavum septi pellucidi
    2. Cavum vergae
    3. Cavum veli interpositi
  2. CYSTIC LESIONS OF POSTERIOR FOSSA
    Evaluate
    • size of 4th ventricle + communication with 4th ventricle
    • size of vermis + cerebellar hemispheres
    • mass effect on cerebellum
    1. Megacisterna magna
    2. Dandy-Walker continuum disorder
    3. Blake pouch cyst
    4. Arachnoid cyst
    5. Vein of Galen malformation
  3. SUPRATENTORIAL PERIVENTRICULAR CYSTS
    1. Connatal cyst
      = coarctation of lateral ventricles + frontal horn cysts
      Location: at / just below superolateral angles of frontal horns / body of lateral ventricles anterior to foramen of Monro
      Cause: normal variant ← approximation of walls of frontal horns; NOT sequelae of ischemia
    2. Subependymal cyst
    3. Choroid plexus cyst
    4. Periventricular leukomalacia
    5. Pseudoporencephaly
  4. SUPRATENTORIAL INTRA- / EXTRAAXIAL CYSTS
    1. Schizencephaly
    2. Ventriculomegaly: hydrocephalus, brain atrophy
    3. Holoprosencephaly
    4. Supratentorial arachnoid cyst
    5. Spontaneous intracranial hematoma
    6. Brain abscess (uncommon)

Cholesterol-containing CNS Lesions!!navigator!!

  1. Epidermoid inclusion cyst
  2. Cholesterol granuloma
  3. Acquired epidermoid of middle ear
  4. Congenital cholesteatoma of middle ear
  5. Craniopharyngioma

Mesencephalic Low-density Lesion!!navigator!!

  1. Normal: decussation of superior cerebellar peduncles at level of inferior colliculi
  2. Syringobulbia
    found in conjunction with syringomyelia, Arnold-Chiari malformation, trauma
    • CSF density centrally
    • intrathecal contrast enters central cavity
  3. Brainstem infarction
    • abnormal contrast enhancement after 1 week
    • well-defined low-attenuation region without enhancement after 2–4 weeks
  4. Central pontine myelinolysis
  5. Brainstem glioma
  6. Metastasis
    • well-defined contrast enhancement
  7. Granuloma in TB / sarcoidosis (rare)

Intracranial Pneumocephalus!!navigator!!

  1. TRAUMA (74%):
    1. blunt trauma
      in 3% of all skull fractures; in 8% of fractures involving paranasal sinuses (frontal >ethmoid >sphenoid >mastoid) or base of skull
    2. penetrating injury
  2. NEOPLASM INVADING SINUS (13%):
    1. Osteoma of frontal / ethmoid sinus
    2. Pituitary adenoma
    3. Mucocele, epidermoid
    4. Malignancy of paranasal sinuses
  3. INFECTION WITH GAS-FORMING ORGANISM (9%) in mastoiditis, sinusitis
  4. SURGERY (4%) hypophysectomy, paranasal sinus surgery
  5. SUPRATENTORIAL CRANIOTOMY
    Location: in any compartment; most often in subdural space over frontal lobe
    Duration after surgery: 2 days (100%), 7 days (75%), 2nd week (60%), 3rd week (26%), >3 weeks (0%)

Mechanism of dural laceration:

  1. ball-valve mechanism during straining, coughing, sneezing
  2. vacuum phenomenon ← loss of CSF

Time of onset: on initial presentation (25%), usually seen within 4–5 days, delay up to 6 months (33%)

Mortality: 15%

Cx:

  1. CSF rhinorrhea (50%)
  2. Meningitis / epidural / brain abscess (25%)
  3. Extracranial pneumocephalus = air collection in subaponeurotic space

Outline