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STEP 5: Neuro PATHOMA > Trauma and Demyelinating D/o > Flashcards

Trauma and Demyelinating D/o Flashcards

1
Q

EPIDURAL HEMATOMA: What is seen on CT? What is the chronology of Sx? What is the fatal complication?

A

LENS SHAPED HEMATOMA
LUCID period -> Rapid recurrent unconsciousness = RAPID PROGRESSION
UNCAL HERNIATION = fatal complication

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2
Q

EPIDURAL HEMATOMA: What is the most common location of trauma causing the epidural hematoma? Which artery is most commonly ruptured?

A

TEMPORAL BONE FRACTURE

Middle meningeal artery rupture

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3
Q

SUBDURAL HEMATOMA: What is most common cause of a subdural hematoma? Second most common cause? What is ruptured? How does this clinical presentation differ from EPIDURAL hematoma? What is the fatal complication?

A

Most common cause = TRAUMA to the head
Second most common cause = BRAIN ATROPHY -> resulting in lengthening of the cortical bridging veins

CORTICAL BRIDGING VEIN = Most commonly ruptured
SLOWER progression of Sx than epidural hematoma - Slower leaking blood

Fatal complication = HERNIATION

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4
Q

What are the 3 types of brain herniations (due to mass effect OR increased ICP)

A
  1. CEREBELLAR TONSILLAR HERNIATION
  2. SUBFALCINE HERNIATION
  3. UNCAL HERNIATION
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5
Q

CEREBELLAR TONSILLAR HERNIATION clinically presents as __?

A

Herniation into foramen magnum -> BRAINSTEM COMPRESSION -> CARDIOPULMONARY ARREST

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6
Q

What is a SUBFALCINE HERNIATION?

A

Herniation of CINGULATE GYRUS under the FALX CEREBRI (separating the left and right hemispheres)

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7
Q

What vascular supply does a SUBFALCINE HERNIATION compress?

A

ANTERIOR CEREBRAL ARTERY COMPRESSION -> ACA Infarct

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8
Q

What is an UNCAL HERNIATION?

A

Herniation of the TEMPORAL LOBE UNCUS under the TENTORIUM CEREBELLI (area between the cerebellum and brainstem)

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9
Q

What 3 structures does an UNCAL HERNIATION compress and what are the associated clinical signs?

A
  1. Compression of CN III - Eyes will move DOWN and OUT, DILATED PUPIL (mydriasis)
  2. Compression of POSTERIOR CEREBRAL ARTERY - Infarction of OCCIPITAL LOBE = CONTRALATERAL HOMONYMOUS HEMIANOPSIA
  3. Pull on and Rupture of PARAMEDIAN ARTERY (running along brainstem) = DURET HEMORRHAGES of brainstem
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10
Q

What is a LEUKODYSTROPHY?

A

Inherited mutations in enzymes necessary for PRODUCTION or MAINTENANCE of myelin

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11
Q

What is the most common LEUKODYSTROPHY? What enzyme is deficient? What accumulates as a result?

A

METACHROMATIC LEUKODYSTROPHY - AR mutation of arylsulfatase -> Sulfatides of myelin can NOT get degraded -> MYELIN accumulates in LYSOSOMES of OLIGODENDROCYTES

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12
Q

Other than a LEUKODYSTROPHY, how can METACHROMATIC LEUKODYSTROPHY be categorized? [HINT: Think organelle]

A

LYSOSOMAL STORAGE DISEASE

Accumulation of myelin that could NOT be degraded in OLIGODENDROCYTE LYSOSOMES

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13
Q

Name the 3 LEUKODYSTROPHIES.

A
  1. METACHROMATIC LEUKODYSTROPHY
  2. KRABBE DISEASE
  3. ADRENLEUKODYSTROPHY
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14
Q

What enzyme is deficient in KRABBE DISEASE? What accumulates as a result? Where does it accumulate?

A

BETA GALACTOCERBROSIDASE - Accumulation of GALACTOCEREBROSIDE in MACROPHAGES

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15
Q

What is the inheritance pattern of METACHROMATIC LEUKODYSTROPHY and KRABBE DISEASE?

A

AUTOSOMAL RECESSIVE

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16
Q

What is impaired in ADRENOLEUKODYSTROPHY? What accumulates as a result? Where does it accumulate?

A

Addition of COENZYME A to long chain fatty acids is impaired -> Accumulation of FATTY ACIDS in ADRENAL GLANDS + BRAIN WHITE MATTER

17
Q

What is the inheritance pattern of ADRENOLEUKODYSTROPHY?

A

X-LINKED

18
Q

What is the etiology of MULTIPLE SCLEROSIS? What is its strongest association?

A

AUTOIMMUNE destruction of MYELIN + OLIGODENDROCYTES

Strongest association with HLA-DR2

19
Q

Like other autoimmune conditions, what is the genetic susceptibility + environmental trigger of MS?

A

GENETIC SUSCEPTIBILITY = HLA-DR2

ENVIRONMENTAL TRIGGER = Location - away from the equator

20
Q

**UW: What is a common INITIAL MANIFESTATION of MS? What is affected?

A

OPTIC NEURITIS- Monocular visual loss with pain on eye movement

**UW DECREASED VISION + PAIN AROUND EYE
Due to involvement of OPTIC NERVE

21
Q

What are other possible structures affected with MS and their associated clinical effect?

A
  1. BRAINSTEM: Vertigo + Scanned Speech (Mimics alcohol intoxication)
  2. LEFT MLF: Inability to do a RIGHTWARD gaze with right nystagmus (From functioning eye) - Right eye CAN look right (CN 6),
  3. PERIVENTRICULAR CEREBRAL WHITE MATTER: Hemiparesis/ Unilateral loss of sensation
  4. SPINAL CORD: LE loss of sensation/weakness
    5: AUTONOMIC NERVOUS SYSTEM: Loss of bowel/bladder/sexual function
22
Q

How is the diagnosis of MULTIPLE SCLEROSIS made (2 Diagnostic Tools)? What are the + results?

A
  1. MRI: Multiple OVOID, white matter lesions
  2. LP: INCREASED LYMPHOCYTES + OLIGOCLONAL IgG bands [high-resolution electrophoresis] + MYELIN BASIC PROTEIN (from myelin destruction and protein leakage)
23
Q

NEUROLOGIC SYMPTOMS THAT PRESENT DISSEMINATED IN TIME AND SPACE = ?

A

MULTIPLE SCLEROSIS

24
Q

What is seen on biopsy of MULTIPLE SCLEROSIS?

A

Loss of myelination = GRAY-APPEARING PLAQUES in the white matter

25
Q

What is the Tx of acute MS attacks?

A

HIGH DOSE STEROIDS

26
Q

What is the long-term Tx of MS?

A

IFN-beta: Slows progression of disease

27
Q

Pt is a an infant who gets a MEASLES VIRUS infection in infancy. Presents with neurologic signs years later during childhood. What is the most likely diagnosis?

A

SUBACUTE SCLEROSING PANENCEPHALITIS

28
Q

What is the hallmark defining feature of SUBACUTE SCLEROSING PANENCEPHALITIS?

A

Subacute, Sclerosing (S,S) = S for SLOWLY progressing, persistent infection of the brain (BOTH WHITE/GRAY MATTER) by MEASLES VIRUS -> Presents with neuro Sx later during childhood -> FATAL

29
Q

What is the diagnostic test confirming SUBACUTE SCLEROSING PANCENPHALITIS?

A

VIRAL INCLUSIONS of MEASLES VIRUS within GRAY MATTER NEURONS + WHITE MATTER OLIGODENDROCYTES

30
Q

What is PROGRESSIVE MULTIFOCAL PANENCEPHATLITIS? What viral infection is it associated with? What is the trigger of this disease?

A

JC (POLYOMAVIRUS) VIRAL INFECTION of OLIGODENDROCYTES (WHITE MATTER - MULTIPLE FOCI)

Normally LATENT infection
REACTIVATION in an immunosuppressed pt (e.g. AIDS or LEUKEMIA pt receiving immunosuppression)

31
Q

What is the classic presentation of PROGRESSIVE MULTIFOCAL PANENCEPHALITIS?

A

PROGRESSIVE = RAPIDLY PROGRESSIVE neurologic sx (vision loss, weakness, dementia) resulting in DEATH

32
Q

What is CENTRAL PONTINE MYELINOLYSIS?

A

FOCAL Demyelination of CENTRAL PONS (anterior brainstem)

33
Q

What is the most common cause of CENTRAL PONTINE MYELINOLYSIS? Who is the typical pt?

A

RAPID IV CORRECTION OF HYPONATREMIA

In severely malnourished pt (LIVER DISEASE, ALCOHOLIC)

34
Q

What is the classic presentation/ syndrome presented with CENTRAL PONTINE MYELINOSIS?

A

LOCKED IN SYNDROME = Acute bilateral paralysis (HEAD ->TOE) except for the EYES

VERTICAL EYE MOVEMENTS + EYELID ELEVATION SPARED (cn 3,4,6 arise from the tegmentum of the midbrain = rostral to the pons)

35
Q

What are the 5 demyelinating disorders?

A
  1. LEUKODYSTROPHY - Metachromatic (myelin in lysosomes), Krabbe (galactocerebroside in macrophages), Adrenoleukodystrophy (fatty acids in adrenal glands + white matter)
  2. MULTIPLE SCLEROSIS - autoimmune [myelin + oligodendrocytes]
  3. SUBACUTE SCLEROSING PANENCEPHALITIS: Measles virus affecting BOTH White/Gray matter
  4. PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY: Re-activation of Latent JC virus affecting White matter multifocally
  5. CENTRAL PONTINE MYELINOSIS: Rapid IV correction of HYPONATREMIA, LOCKED IN SYNDROME

STEP 5: Neuro PATHOMA (6 decks)

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