Intracranial Diseases part 1 Flashcards

1
Q

structures considered to be in the supratentorial region of the brain

A
  • Telencephalon
  • Diencephalon
  • CN 1-2
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2
Q

structures considered to be in the infratentorial region of the brain

A
  • Mesencephalon
  • Metencephalon
  • Myelencephalon
  • CN 3-12
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3
Q

Supratentorial Signs

A
  • Contralateral paresis > ipsilateral – usually minimal
    gait deficits
  • Contralateral CP deficits > ipsilateral deficits (UMN)
  • Contralateral menace deficit (cortical blindness -
    avisual)
  • Contralateral facial response deficit
  • Contralateral hemi-neglect sydrome
  • Ipsilateral circling
  • Ipsilateral head turn
  • Seizures
  • Behavioral changes / altered mental status
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4
Q

Infratentorial Signs

A

􀂄􀂄 Ipsilateral paresis > contralateral – can have
severe gait deficits
􀂄􀂄 Ipsilateral CP deficts > contralateral (UMN)
􀂄􀂄 Ipsilateral cranial nerve deficits (III-XII) - except
trochlear nerve (CN IV) which is contralateral
􀂄􀂄 Cerebellar / vestibular signs
􀂄􀂄 Postural abnormalities
􀃆􀃆 decerebrate rigidity
􀃆􀃆 decerebellate rigidity
􀂄􀂄 Abnormal respiratory pattern
􀂄􀂄 Altered mental status 􀃆􀃆 RAS abnormality

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5
Q

Top 5 Intracranial Differentials

A
􀂄􀂄 Hydrocephalus
􀂄􀂄 Meningitis / encephalitis
􀂄􀂄 Tumor
􀂄􀂄 Cerebral Vascular Accident (CVA)
􀂄􀂄 Trauma
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6
Q

Differentials for Degenerative Diseases

A
􀂄􀂄 Storage diseases
􀂄􀂄 Leukodystrophy
􀂄􀂄 Neuroaxonal dystrophy
􀂄􀂄 Dysmyelination
􀂄􀂄 Cerebellar abiotrophy
􀂄􀂄 Age-related degeneration / cognitive dysfunction
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7
Q

Differentials for “Anomalous” disease

A
􀂄􀂄 Hydrocephalus
􀂄􀂄 Hydrancephaly
􀂄􀂄 Lissencephaly
􀂄􀂄 Cerebellar hypoplasia
􀂄􀂄 Caudal Occipital Malformation Syndrome
(COMS)
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8
Q

Hydrocephalus

A

Abnormal dilation

of the ventricles

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9
Q

Congenital hydrocephalus is most commonly due to what defect?

A

Most commonly due
to stenosis of the
mesencephalic
aqueduct

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10
Q

Breeds predisposed congenital hydrocephalus?

A

Chihuahua, pugs,
maltese, boston
terrier, yorkies…etc

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11
Q

Physical apperance of hydrocephalus

A

Dome-shaped head
Persistent fontanels
Ventral / lateral
strabismus

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12
Q

Clinical signs of congenital hydrocephalus

A
Usually supratentorial
- poor learners
- behavioral changes
- visual deficits
- circling
- seizures
\+/- infratentorial signs
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13
Q

Diagnosis of Congenital Form of hydrocephalus

A

-Signalment - breed
-Clinical signs
Imaging
Ultrasound
CT
MRI
CSF analysis – rule
out inflammatory
disease

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14
Q

Treatment of congenital hydrocephalus

A
Prednisone therapy – decrease CSF production
 Diuretics – acetazolamide, mannitol
 Omeprazole
 Ventricular CSF shunting
 infections
 undershunting / overshunting
 mechanical failure / obstruction
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15
Q

Hydrancephaly

A
Cerebral hemisphere
reduced to fluid-filled
sac
 Meninges and
ependyma intact
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16
Q

Animals that often get hydracephaly

A

Panleukopenia

(distemper) in kittens

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17
Q

Lissencephaly

A

􀂄􀂄 “smooth brain”
􀂄􀂄 Minimal sulci / gyri
􀂄􀂄 Due to abnormal cerebral cortical neuronal
migration during fetal development

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18
Q

What breeds (cats and dogs) are associated with lissencephaly?

A

Lhasa Apso dogs, Wire-Haired Fox Terrier, Irish
Setter
Korat cats

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19
Q

Cerebellar Hypoplasia is most often due to what?

A
Viral infection in utero or first
few weeks of life:
- cats: distemper (parvovirus)
- dogs: herpesvirus?
parvovirus?
Congenital
20
Q

Caudal Occipital Malformation

Syndrome (COMS) - Clinical Signs

A
- Analogous to Chiari type I malformation in
humans
- Malformation of the caudal occipital area
-  Overcrowding of the caudal fossa
- Cerebellar compression and herniation
- Focal meningeal hypertrophy at foramen
magnum
- Increase CSF pressure 􀃆􀃆 hydrocephalus
- Concurrent syringohydromyelia
21
Q

Treatment options for COMS

A
􀂄􀂄 Prednisone therapy
􀂄􀂄 +/- omeprazole
􀂄􀂄 +/- gabapentin
􀂄􀂄 Surgery – Foramen magnum
decompression
22
Q

Signalment for COMS

A

􀂄􀂄 Small breed dogs, specifically CKCS
􀂄􀂄 Mean age at time of surgery 3.9 years
(10m-9yrs)

23
Q

Clinical Signs of COMS

A
􀂄􀂄 Scratching behavior*
􀂄􀂄 Spinal pain
􀂄􀂄􀂄􀂄 Paresis to paralysis / CP deficits
􀂄􀂄 Diminished menace response (visual)
􀂄􀂄 Vestibular-Cerebellar signs
􀂄􀂄 Seizures
􀂄􀂄 Paraspinal atrophy 􀃆􀃆 scoliosis
- most likely due to the syrinx
24
Q

Differentials for Metabolic Encephalopathy

A
Liver disease (hepatic encephalopathy)
 Renal encephalopathy
 Glucose abnormalities
 Electrolyte abnormalities – Ca, Na, K
 Hypertriglyceridemia
 Thyroid abnormalities
 Adrenal abnormalities
25
Q

Clinical Clues to Metabolic

Encephalopathies

A
Episodic signs – wax and wane
PE abnormalities
- hepatomegaly, icterus
- uremic breath
- abnormal body condition
- Skin abnormalities
Typically symmetric neurologic deficits
26
Q

Hypoglycemia

A
Mental alteration –
dullness to coma
 Irritability
 Pupillary dilation
 Seizures
 Tremors
 Generalized weakness
 Visual deficits
27
Q

Mechanisms for the clinical signs of hypoglycemia

A

Mechanisms:

  1. Neuroglycopenia
  2. Sympathetic nervous
28
Q

Mechanism of hypernatremia induced encephalopathy

A

Hypernatremia 􀃆􀃆 hyperosmolality 􀃆􀃆
shrinkage of brain cells 􀃆􀃆 stretching and
tearing of small brain blood vessels 􀃆􀃆
hemorrhage
􀂄􀂄 With chronicity (>2-3 days), brain cells will
produce idiogenic osmoles to compensate for
extracellular hyperosmolality

29
Q

Mechanism of hyponatremia induced encephalopathy

A

Hyponatremia > hypoosmolality > swelling

of brain cells > brain edema

30
Q

Sequelae to too rapid correction of chronic hypernatremia

A

cerebral edema

31
Q

Sequelae to too rapid correction of chronic hyponatremia

A

thalamic myelinolysis,

brain cell dehydration, hemorrhage

32
Q

Safe correction rate of sodium

A

< 0.5 meq / L / hour

33
Q

Hypothyroidism causes what cranial nerve deficits and subsequently, what clinical signs?

A
  • CN 5, 7, 8 dysfunction
  • decrease facial sensation
  • facial paralysis
  • vestibular dysfunction – head tilt, circling, strabismus,
    nystagmus
34
Q

Clinical signs of hypotheryoidism

A

􀂄􀂄 Laryngeal paralysis, megaesophagus
􀂄􀂄 Appendicular neuropathy
􀂄􀂄 Has been linked to myasthenia gravis
􀂄􀂄 Hypertension (atherosclerosis) 􀃆􀃆 cerebral vascular accident
􀂄􀂄 Myopathy - typically subclinical
􀂄􀂄 Myxedematous stupor / coma – rare, life-threatening,
Doberman Pinschers

35
Q

Clinical signs of hyperthyroidism

A
Restlessness, irritable, aggressive,
wandering, pacing, circling
 Seizures
 Cerebral vascular accidents (hypertension)
 Muscle weakness – tremors, ventral neck
flexion – due to hypoK
36
Q

Myopathy associated with hyerpadrenocorticism

A

Myopathy – type II
muscle atrophy,
myotonia

37
Q

Vascular changes associated with hyperadrenocorticism

A

systemic hypertension- increased hypercoagulability

38
Q

Neurologic signs associated with hyperadrenocorticism

A
Local tumor expansion
(macroadenoma) -->
mental alteration,
seizures, blindness
-Nelson’s syndrome --> acute neurologic dysfunction following adrenolytic therapy
-Hydrocephalus ex vacuo due to
corticosteroid-induced
neuronal damage
39
Q

Thiamine (Vit B1) Deficiency Causes

A
  • Lack of intake
  • Thiaminase (all fish diet)
  • Overcooking meat
40
Q

Thiamine (Vit B1) Deficiency - species most commonly affected

A

cats

41
Q

In cats what brain regions are affected by B1 deficiency

A

Polioencephalomalacia – bilateral occulomotor,

vestibular, lateral geniculate nuclei, caudal colliculus

42
Q

Clinical signs of Thiamine/Vit B1 deficiency?

A
  • CS are acute and rapidly progressive - lethargy,
    inappetence, dilated pupils, vestibular signs, visual
    deficits, ventral neck flexion, coma, opisthotonus,
    death
43
Q

In dogs what brain regions can also be affected by B1 deficiency

A
  • Dogs – cerebellum and cerebral cortex can be

affected

44
Q

Treatment of Thiamine (Vit B1) deficiency?

A
  • TX – IV/IM/SQ thiamine hydrochloride

- Prognosis good if treated early in disease

45
Q

mean age for intracranial neoplasia

A

> 5 years of age – median 9

46
Q

gliomas common in what breed?

A

brachycephalics