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Neurology > Intracranial disease > Flashcards

Intracranial disease Flashcards

1
Q

Telencephalon - what is it?

A
  • Cerebral cortex
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2
Q

Diencephalon - what is it?

A
  • Hypothalamus, thalamus, and pituitary
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3
Q

Mesencephalon - what is it?

A
  • Midrain
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4
Q

Metencephalon - what is it?

A
  • Cerebellum and brainstem
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5
Q

Myelencephalon - what is it?

A
  • Medulla oblongota
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6
Q

Supratentorial structures

A
  • Telencephalon
  • Diencephalon
  • CN 1-2
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7
Q

Infratentorial structures

A
  • Mesencephalon
  • Metencephalon
  • Myelencephalon
  • CN 3-12
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8
Q

Where is the functional cross-over?

A
  • Mesencephalon
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9
Q

Supratentorial signs:

Which are contralateral and which are ipsilateral?

A
  • Contralateral Paresis (more often than ipsilateral; often still ambulatory)
  • Contralateral CP deficits (more often than ipsilateral deficits; UMN)
  • Contralateral Menace deficit (cortical blindness - avisual)
  • Contralateral Facial response deficit
  • Contralateral Hemi-neglect syndrome
  • Ipsilateral Circling
  • Ipsilateral Head turn
  • Seizures
  • Behavior changes/altered mental status (mild)
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10
Q

Infratentorial signs

  • and which are ipsilateral/contralateral?
A
  • Ipsilateral paresis > contralateral - can have severe gait deficits (nonambulatory)
  • Ipsilateral CP deficits > contralateral (UMN)
  • Ipsilateral CN deficits (III-XII) except trochlear nerve (CN IV) which is contralateral
  • Cerebellar/vestibular signs
  • Decerebrate or decerebellate rigidity
  • Abnormal respiratory pattern
  • Altered mental status (severe) –> RAS abnormality
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11
Q

Which CN is contralateral infratentorial?

A
  • CN IV (trochlear nerve)
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12
Q

What signs are common to both cerebellar and vestibular lesions?

A
  • Head tilt (paradoxical)
  • Nystagmus/ocular tremors
  • Falling/wide-based stance/rolling
  • Ataxia
  • Circling
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13
Q

Characterize the cerebellar ataxia?

A
  • Hypermetria ataxia
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14
Q

What signs are unique to cerebellar and could help you distinguish from vestibular?

A
  • Tremor (intention, head or generalized)
  • Menace deficit that is ipsilateral BUT VISUAL
  • Rebound phenomenon
  • Cerebellate rigidity
  • Elevated 3rd eyelid, pupillary dilation, enlarged palpebral fissures
  • Increase urination
  • NO CP deficits or paresis
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15
Q

What signs are unique to vestibular and could help you distinguish from cerebellar?

A
  • Head tremors and eyelid contraction both secondary to nystagmus
  • Positional strabismus
  • +/- CP deficits or paresis (>ipsilateral)
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16
Q

What four things are unique to central vestibular lesions and you should know???***

A
  • Vertical nystagmus
  • Changing nystagmus
  • Other CN deficits other than 7 or 8
  • CP deficits
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17
Q

What are the two localizations of a head tilt?

A
  • Cerebellar

- Vestibular

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18
Q

Where does circling localize?

A
  • Cerebellar
  • Vestibular
  • Supratentorial
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19
Q

Where does positional strabismus with no resting strabismus localize?

A
  • Vestibular dysfunction!
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20
Q

Where do intention tremors localize?

A
  • Cerebellar
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21
Q

WHere does the rebound phenomenon localize?

A
  • Cerebellar
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22
Q

Localize:

R head tilt, falling to the R, circling to the R

A
  • Right vestibular
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23
Q

DAMNITV

A
  • D (degenerative)
  • A (anomalous)
  • M (metabolic)
  • N (neoplastic, nutritional)
  • I (inflammatory from infection or not)
  • T (trauma, toxicity
  • V (vascular
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24
Q

Top 5 Intracranial differentials (KNOW)

A
  • Hydrocephalus
  • Meningitis/encephalitis
  • Tumor
  • Cerebral vascular accident (CVA)
  • Trauma
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25
Q

Degenerative neuro disease definition

A
  • failure of neural elements to survive –> primary intracellular pathophysiologic defect (enzyme or something)
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26
Q

Examples of degenerative neuro diseases

A
  • Storage diseases
  • Leukodystrophy
  • Neuroaxonal dystrophy
  • Dysmyelination
  • Cerebellar abiotrophy
  • Age-related degeneration/cognitive dysfunction
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27
Q

Clinical clues to degenerative diseases

Signalment

A
  • Age, sex, breed

- Often weeks to months old

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28
Q

Clinical clues to degenerative diseases

Disease course

A
  • Progressive!
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29
Q

Clinical clues to degenerative diseases

Painful or not?

A
  • Not painful
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30
Q

Clinical clues to degenerative diseases

Localization?

A
  • Often multifocal or widespread clinical signs
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31
Q

What degenerative diseases can lead to organomegaly?

A
  • Storage diseases
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32
Q

Localization:

  • Slowly progressive over the last 6 months
  • Personality change
  • Loss of learned behavior
  • Tetraparesis with CP deficits (UMN)
  • Ataxia - Hypermetria
  • Menace deficit but visual
A
  • Supratentorial with cerebellum
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33
Q

What are two localizations for a menace deficit that is visual?

A
  • CN VII or cerebellum
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34
Q

Describe the typical answer of each for ceroid lipofuscinosis (Batten’s disease)

  • Progression of clinical signs
  • Pain
  • MRI
  • CSF
  • Diagnosis
A
  • Slowly progressive
  • Non-painful
  • MRI showed mild bilateral cortical atrophy, hydrocephalus
  • CSF was normal
  • Dagnosis: Urine metabolic screening and ultimately Histopathology
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35
Q

Anomalous differentials

A
  • Hydrocephalus
  • Hydrancephaly
  • Lissencephaly
  • Cerebellar hypoplasia
  • Caudal occipital malformation syndrome
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36
Q

Hydrocephalus definition

A
  • Abnormal dilation of the ventricles
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37
Q

Hydrocephalus general cause categories?

A
  • Congenital vs acquired
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38
Q

Label the ventricles

A
  • Just do it
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39
Q

What is most common cause of congenital hydrocephalus?

A
  • Stenosis of the mesencephalic aqueduct
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40
Q

Breeds predisposed to congenital hydrocephalus

A
  • Chihuahuas
  • pugs
  • Maltese
  • Boston Terrier
  • Yorkies
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41
Q

Appearance with congenital hydrocephalus

A
  • Dome-shaped head
  • Persistent fontanels (soft spot in the skull where the sutures didn’t come together)
  • Ventral/lateral strabismus
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42
Q

Clinical signs of congenital hydrocephalus

A
  • Supratentorial signs usually
  • Poor learners
  • Behavioral changes
  • Visual deficits
  • Circling
  • Seizures
  • +/- infratentorial signs
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43
Q

Diagnosis of congenital hydrocephalus

A
  • SIgnalment (breed)
  • Clinical signs
  • Imaging (U/S, CT, MRI)
  • CSF analysis to rule out inflammatory disease
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44
Q

Prognosis for congenital hydrocephalus

A
  • Extremely guarded
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45
Q

Treatment for congenital hydrocephalus

A
  • Prednisone therapy to decrease CSF
  • Diuretics (acetazolamide, mannitol, furosemide)
  • Omeprazole to decrease CSF production
  • Ventricular CSF shunting
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46
Q

Complications of ventricular CSF shunting

A
  • Infections
  • Undershunting or overshunting
  • Mechanical failure or obstruction
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47
Q

Are all hydrocephalic dogs clinical?

A
  • No
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48
Q

Hydrancephaly definition

A
  • Cerebral hemisphere reduced to fluid-filled sac

- Meninges and ependyma intact

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49
Q

What can cause hydrancephaly in kittens?

A
  • Panleukopenia (distemper) in kittens
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50
Q

Lissencephaly definition

A
  • Smooth brain

- Minimal sulci/gyri

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51
Q

WHat causes lissencephaly?

A
  • Abnormal cerebral cortical neuronal migration during fetal development
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52
Q

WHich breeds get lissencephaly?

A
  • Lhasa apso dogs
  • Wire-haired fox Terrier
  • Irish Setter
  • Korat cats
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53
Q

Signs of lissencephaly

A
  • Seizures
  • Poor learning
  • BLindness
  • Typically non-progressive
  • Non-fatal
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54
Q

What is cerebellar hypoplasia?

A
  • Abnormal development of the cerebellum
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55
Q

What can cause cerebellar hypoplasia in dogs and cats?

A
  • Viral infection in utero or first few weeks of life
  • Cats: Distemper (Parvovirus)
  • Dogs: Herpesvirus? Parvovirus?
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56
Q

WHo gets developmental cerebellar hypoplasia and lissencephaly?

A
  • Wire Haired Fox Terriers

- Irish Setters

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57
Q

Signs of cerebellar hypoplasia?

A
  • CSF first when tries to stand and walk

- Non-progressive if survives systemic signs of viral infection

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58
Q

How can you tell apart cerebellar hypoplasia vs cerebellar abiotrophy?

A
  • Cerebellar abiotrophy will get worse

- Cerebellar hypoplasia may improve or shouldn’t progress

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59
Q

Localization:

  • Decreased CP in the pelvic limbs and the left thoracic limb
  • Normal spinal reflexes
  • Normal cranial nerves
  • Normal cutaneous trunci
  • No palpable spinal pain
A
  • C1-C5 (left sided)
  • Infratentorial left sided
  • Supratentorial right sided
  • UMN CP deficits L>R
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60
Q

Top 5 intracranial differentials again

A
  • Hydrocephalus
  • Meningitis/Encephalitis
  • Vascular accident
  • Tumor
  • Exogenous trauma
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61
Q

Top 5 spinal dfdx

A
  • IVDD
  • Meningitis/myelitis
  • Discospondylitis
  • Tumor
  • Exogenous trauma
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62
Q

Caudal occipital malformation syndrome name in humans

A
  • Chiari type I malformation
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63
Q

What is caudal occipital malformation syndrome?

A
  • Malformation of the caudal occipital area

- Overcrowding of the caudal fossa

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64
Q

Consequences of caudal occipital malformation syndrome

A
  • Cerebellar compression and herniation
  • Focal meningeal hypertrophy at the foramen magnum
  • Increase CSF pressure –> hydrocephalus
  • Concurrent syringohydromyelia (fluid accumulation down the spinal cord; like hydrocephalus in the spinal cord)
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65
Q

Diagnostic plan for suspected caudal occipital malformation syndrome?

A
  • Advanced imaging

- +/- CSF analysis +/- cultures and titers

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66
Q

Appearance on MRI of COMS

A
  • Skull causes a little indentation
  • CSF that normally goes down the fourth ventricle and down the central canal is obstructed
  • White cavity down the spinal cord that is either fluid or fat and turns black with FLAIR sequence
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67
Q

Syringohydromyelia

A
  • CSF accumulation within the spinal cord

- Can involve the central canal

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68
Q

Hydromyelia

A
  • Cavity within the parenchyma not involving the central canal
  • If it breaks into the central canal it’s syringohydromyelia?
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69
Q

Treatment options for COMS

A
  • Prednisone therapy
  • +/- omeprazole
  • +/- .l;’’’’’’’’’’’’’]]]]],kgabapentin for pain
  • Surgery
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70
Q

What surgery for treatment of COMS

A
  • Foramen magnum decompression
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71
Q

Signalment for COMS

A
  • Small breed dogs, specifically CKCS

- Mean age at time of surgery 3.9 years

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72
Q

Clinical signs of COMS

A
  • Scratching behavior**
  • Spinal pain
  • Paresis to paralysis/CP deficits
  • Diminished menace response (visual) - cerebellar
  • Vestibular-Cerebellar Signs
  • Seizures (2° to hydrocephalus)
  • Paraspinal atrophy (scoliosis; most likely due to the syrinx)
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73
Q

Why do dogs with COMS scratch?

A
  • No on really knows
  • Syrinx affects pain and sensory pathways
  • Leads to pain and paresthesia of the corresponding dermatomes
  • Abnormal skin perception
  • Intolerant to touching and neck collars
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74
Q

Metabolic causes of neurologic disease

A
  • Liver disease (hepatic encephalopathy)
  • Renal encephalopathy
  • Glucose abnormalities
  • Electrolyte abnormalities (Ca, Na, K)
  • Hypertriglyceridemia
  • Thyroid abnormalities
  • Adrenal abnormalities
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75
Q

Clinical clues to metabolic encephalopathies

A
  • Episodic signs that wax and wane
  • PE abnormalities that depend on underlying disease (hepatomegaly, icterus, uremic breath, abnormal body condition, skin abnormalities)
  • Typically symmetric neurologic deficits
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76
Q

What are the toxins with hepatic encephalopathy?

A
  • GABA, aromatic acid, mercaptans, skatoles, ammonia
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77
Q

Pathophysiology of hepatic encephalopathy

A
  • Toxic to white matter (oligos) –> demyelination

- Toxic to gray matter (basal nuclei) –> ischemic neuron

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78
Q

Signs with hepatic encephalopathy in dogs

A
  • Typically supratentorial
  • Obtundation
  • Abnormal behaviors
  • Head-pressing
  • Visual deficits
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79
Q

Signs with hepatic encephalopathy in cats

A
  • Ptyalism
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80
Q

When can clinical signs be worse with hepatic encephalopathy?

A
  • After eating
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81
Q

MRI with hepatic encephalopathy

A
  • Widened sulci

- Lentiform nuclei

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82
Q

Hypoglycemia clinical signs

A
  • Mental alteration (dullness to coma)
  • Irritability
  • Pupillary dilation
  • Seizures
  • Tremors
  • Generalized weakness
  • Visual deficits
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83
Q

Glucose levels where we worry about seizures

A
  • <30 mg/dL for sure

- Worry at <50 mg/dL

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84
Q

Mechanisms of clinical signs with hypoglycemia

A
  1. neuroglycopenia

2. Sympathetic nervous system stimulation

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85
Q

Hypernatremia pathophysiology

A
  • 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
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86
Q

Idiogenic osmoles

A
  • With chronicity (>2-3 ays) brain cells produce idiogenic osmoles to compensate for extracellular hyperosmolality
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87
Q

Hyponatremia pathophysiology?

A
  • Hypoosmolality –> swelling of brain cells –> brain edema
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88
Q

What happens if you correct chronic hypernatremia too rapidly?

A
  • Cerebral edema
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89
Q

What happens if you correct chronic hyponatremia too rapidly?

A
  • Thalamic myelinolysis
  • Brain cell dehydration
  • Hemorrhage
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90
Q

What is the safe rate of correction with sodium?

A
  • <0.5 mEq/L/hr
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91
Q

Hypothyroidism - which neurologic signs can be seen?

A
  • CN 5, 7, and 8 (decreased facial sensation, facial paralysis, vestibular dysfunction with head tilt, circling, strabismus, nystagmus)
  • Laryngeal paralysis, megaesophagus (CN 10 dysfunction)
  • Appendicular neuropathy
  • Myasthenia gravis
  • Cerebral vascular accident (2° to hypertension and cerebral vascular accident)
  • Myopathy (typically subclinical
  • Myxedematous stupor
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92
Q

WHat is myxedematous stupor?

A
  • Rare, life-threatening

- Doberman Pinschers get it

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93
Q

Hyperthyroidism neurologic signs

A
  • Restlessness, irritable, aggressive, wandering, pacing, circling
  • Seizures
  • Cerebral vascular accidents (hypertension)
  • Muscle weakness - tremors, ventral neck flexion due to hypokalemia
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94
Q

Hyperadrenocorticism possible clinical signs

A
  • Myopathy (type II muscle atrophy, myotonia)
  • Neuropathy
  • SYstemic hypertension and hypercoagulability lead to CVAs
  • Hydrocephalus ex vacuo due to corticosteroid induced neuronal damage
  • Local tumor expansion (macroadenoma) leading to mental alteration, seizures, blindness
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95
Q

WHat is Nelson’s syndrome?

A
  • Acute neurologic dysfunction following adrenolytic therapy
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96
Q

Cushings Myotonia

A
  • Failure of the muscles to relax

- Inappropriate tone in the muscle

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97
Q

Sound of myotonic potentials on EMG

A
  • Dive bombers
  • You can hear the muscle fire
  • Waxing and waning
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98
Q

Thiamine deficiency - how can it happen?

A
  • Lack of intake (anorexic for a LONG time)
  • Thiaminase (all fish diet)
  • Overcooking meat
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99
Q

Which species is most affected by Thiamine deficiency?

A
  • Cats
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100
Q

Lesions associated with thiamine deficiency

A
  • Polioencephalomalacia
  • Bilateral oculomotor, vestibular, lateral geniculate nuclei
  • Caudal colliculus
  • In dogs, the cerebellum and cerebral cortex can be affected
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101
Q

Clinical signs associated with thiamine deficiency

A
  • Acute and rapidly progressive
  • Lethargy
  • Inappetence
  • Dilated pupils
  • vestibular signs
  • Visual deficits
  • Ventral neck flexion
  • Coma
  • Opisthotonus
  • Death
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102
Q

Treatment of thiamine deficiency

A
  • IV/IM/SQ thiamine hydrochloride
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103
Q

Prognosis for thiamine deficiency

A
  • Good if treated earlier in the disease
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104
Q

Typical age of neoplasia

A
  • > 5 years of age with a median of 9
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105
Q

Most common clinical signs of neoplasia

A
  • Seizures are the most common

- Behavioral changes after that

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106
Q

Most common tumor in dogs and cats

A
  • Meningiomas
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107
Q

Who gets gliomas?

A
  • Brachycephalic breeds
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108
Q

Where are choroid plexus tumors?

A
  • Associated with ventricle
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109
Q

Paraneoplastic syndromes associated with pituitary tumors?

A
  • Hyperadrenocorticism

- Acromegaly

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110
Q

Tumors that can metastasize to the brain?

A
  • Hemangiosarcoma
  • Lymphosarcoma
  • Carcinomas
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111
Q

Neurologic localization:

  • Dull mental status, head pressing
  • Wide circles to the right
  • Left menace deficit (avisual)
  • Tetraparesis, L>R
  • Normal spinal reflexes
A
  • Right supratentorial
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112
Q

Diagnostic plan for a suspected tumor?

A
  • Metabolic workup (CBC/Chem/UA)
  • Thoracic radiographs to rule out metastasis
  • SErial systolic blood pressures
  • Thyroid status
  • Advanced imaging (MRI or CT)
  • +/- CSF analysis/cultures/titers
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113
Q

MRI appearance of meningiomas

A
  • Extra-axial
  • Broad-based attachment
  • Contrast enhancing
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114
Q

What is the most common brain tumor in dogs and cats?

A
  • Meningioma
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115
Q

Where do meningiomas arise from?

A
  • Arachnoid layer between dura and pia mater
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116
Q

Behavior of meningiomas most often

A
  • Usually histopathologically benign

- Extraneural metastasis are rare

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117
Q

Meningiomas in cats

A
  • Well-encapsulated, firm, easily removable

- Can have multiple masses

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118
Q

Meningiomas in dogs

A
  • Usually solitary, meshwork of vessels internally, intimately attached to the underlying tissue (more difficult to remove)
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119
Q

Treatment of meningiomas (medical vs surgical)

  • What do they recommend here?
A
  • Corticosteroid to decrease edema/inflammation in the brain secondary to the tumor
  • Chemotherapy (hydroxyurea)
  • Radiation therapy
  • Surgery
  • Surgery + radiation therapy**
  • Surgery and hydroxyurea
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120
Q

Prognosis for meningioma in cats

A
  • If they have surgery, often can be curative

- 22-27 months but often die of other things

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121
Q

Prognosis for meningioma in dogs

A
  • Median survival with surgery is 7 months
  • With radiation therapy is 1-2 years
  • With both is 3 years
  • Often infiltrating tumors so hard to completely cure
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122
Q

Localize:

Right sided CP deficits

Normal spinal reflexes

R masseter/temporalis muscle atrophy

Decreased facial sensation on R

Decreased ocular sensation on R

  • Corneal ulcer on the R
A
  • R sided trigeminal nerve

- May involve all three branches (ophthalmic, maxillary, and mandibular branch)

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123
Q

WHat causes neurotropic keratitis?

A
  • Lack of corneal sensation (CN5 ophthalmic) –> lack of reflex tears (CN7)
  • Ophthalmic branch provides homeostasis and nutrition for the cornea
124
Q

Dfdx for CN V deficits that are unilateral and severe

A

**TUMOR (nerve sheath tumor, lymphosarcoma, myelomonocytic leukemia)

  • Infectious/granuloma –> toxoplasma, neospora
  • Trauma
125
Q

Dfdx for bilateral atrophy of the muscles of mastication

A
  • Trigeminal neuritis that is idiopathic
126
Q

Diagnostic plan for suspected tumor associated with CN V deficits

A
  • CBC/Chem/UA
  • Thoracic radiographs (met check)
  • Brain MRI (better than CRI)
  • +/- CSF
  • +/- surgical biopsy
127
Q

Appearance of nerve sheath tumor on MRI

A
  • In the area of CNV

- There’s a special contrast

128
Q

Treatment options for nerve sheath tumors

A
  • Surgical resection (technically difficult, difficult to get clean margins, cosmetic consequences)
  • Fractionated radiation therapy
  • Radiosurgery (<2 cm)
129
Q

Prognosis for nerve sheath tumors

A
  • Limited in literature
  • 12 months in nontreated dogs
  • Surgery (alive at 27 months in one dog)
  • Radiation?
  • Don’t die of CN deficit but eventually lose ability to walk
130
Q

What tumors tend to be at the cerebellomedullary junction?

A
  • Meningioma
  • Choroid plexus tumor
  • Nerve sheath tumor (NST)
131
Q

Pituitary macroadenoma location

A
  • Sella or area of the pituitary

- Takes up contrast quite well

132
Q

What makes a pituitary macroadenoma technically a macroadenoma?

A
  • > 1 cm in height
133
Q

Appearance of pituitary macroadenoma on MRI

A
  • Sella or suprasellar location
  • > 1 cm, expands into diencephalon
  • Contrast enhancing
134
Q

Treatment for pituitary macroadenoma

A
  • Fractionated radiation therapy (18 treatments at 2.5 Grays)
  • Radiosurgery (<2 cm)
  • Median survival ~1-2 years
  • Transphenoidal hypophysectomy (done here)
135
Q

What is the name for the special surgery they do here?

A
  • Transphenoidal hypophysectomy
136
Q

Approach for transphenoidal hypophysectomy

A
  • They go transphenoidally through the soft palate
  • Go into the basosphenoid bone
  • Incise into the dura
  • Usually mucinous and melt out
137
Q

Dfdx for what looks like a hematoma on MRI?

A
  • Hematoma
  • Hemangiosarcoma
  • Make sure the dog isn’t anemic and no coagulopathy
138
Q

Metastatic hemangiosarcoma - what should you do if you suspect based on appearance of MRI

A
  • Screen the abdomen
139
Q

Necropsy appearance of metastatic hemangiosarcoma

A
  • Multifocal masses

- Sometimes you’ll only see the primary mass on MR

140
Q

MAF brain biopsy

A
  • Try to get a sample for histopath
  • Trying to get a sample first to determine treatment plan
  • These allow you to get really bright circles and can relocate that spot later on to develop three-way planning
141
Q

Tocagen gene therapy

A
  • Murine leukemia virus (MLV) to deliver the cytosine deaminase gene
  • MLV should technically only replicate in dividing cells so should not affect surrounding brain
  • Once teh gene is in the brain tumor cells, cytosine deaminase can then convert 5-FC (oral antifungal drug) to 5-FU which can kill cancer cells
  • Worked well for glial cell tumors but not meningiomas
142
Q

Broad categories of inflammatory neuro disease?

A
  • Infectious vs non-infectious
143
Q

Localization of inflammatory neuro disease?

A
  • Multifocal, diffuse nervous signs
144
Q

Other signs associated with inflammatory neuro disease?

A
  • Polysystemic signs including fever
  • Neck pain and diffuse spinal pain
  • Ocular changes!
145
Q

What are the broad categories of infectious disease in the brain?

A
  • Bacterial
  • Viral
  • Protozoal
  • Fungal
  • Algae
  • Parasites
  • Rickettsial
  • Protozoal
146
Q

Bacterial causes of meningitis/encephalitis/neuritis

A
  • 2° to endocarditis
  • Pyometra
  • Foreign body
  • Nasal passages
  • Middle ear
147
Q

Fungal causes of meningitis/encephalitis/neuritis

A
  • Cryptococcosis in cats
  • Blastomycoses
  • Coccidiomycosis
148
Q

Viral causes of meningitis/encephalitis/neuritis

A
  • Distemper
  • Herpes
  • Parvo
  • Parainfluenza
  • Rabies
  • FIP
  • FIV
149
Q

What should you do if an animal is neuro and doesn’t have a good vax history?

A
  • Technically should be quarantining for 7 days
150
Q

Protozoal causes of meningitis/encephalitis/neuritis

A
  • Toxoplasma

- Neospora

151
Q

Rickettsial causes of meningitis/encephalitis/neuritis

A
  • Ehrlichia

- RMSF (vestibular)

152
Q

Parasitic causes of meningitis/encephalitis/neuritis

A
  • Cuterebra
  • Toxocara
  • Heartworm
153
Q

Algal causes of meningitis/encephalitis/neuritis

A
  • Prototheca
154
Q

What type of virus is distemper?

A
  • Paramyxovirus?
155
Q

What happens to the paw pads with distemper virus?

A
  • Hyperkeratotic pads
156
Q

Lesions and signs in younger dogs: Distemper

A
  • Polioencephalomyelopathy
  • SEizures
  • Rarely survive
  • Also respiratory signs
157
Q

Lesions and signs in older dogs with Distemper

A
  • Leukoencephalomyelopathy
  • Older dogs, less severe
  • Brainstem/cerebellar/vestibular signs
  • May develop myoclonus
158
Q

Myoclonus

A
  • Rhythmic, repetitive movement of a group of muscles, present even under anesthesia
159
Q

Localization:

CC Cluster seizures

Obtunded

  • Tetraparesis L>R
  • Normal reflexes
  • Left menace deficit (avisual)
A
  • Right sided supratentorial
160
Q

Treatment for infectious meningitis

A
  • Craniectomy, culture, lavage
  • ANtibiotics
  • Any drug should get into the brain with inflammation
  • She picks cidal over static
161
Q

Do you usually have to put the skull back with a craniectomy?

A
  • No

- Only have to put the skull back if they cross midline

162
Q

Localization

Seizures

Depressed, dull

Nonambulatory tetraparesis

CP deficits in all four limbs

Normal reflexes

Painful neck

A
  • SUpratentorial

- C1-C5 because the neck is painful too (Central cord syndrome)

163
Q

Describe the central cord syndrome again?

A
  • Somatotropic organization
  • Lesion always wrapping around more centrally because it’s knocking out the thoracic limb tracts before pelvic limb tracts
164
Q

Appearance of cryptococcus in CSF

A
  • Non-staining haloes
165
Q

What should you think with eosinophils in CSF?

A
  • Think parasites

- It’s NOT NORMAL

166
Q

Treatment for cryptococcus

A
  • Fluconazole (antifungal drug that crosses BBB)
  • Cage rest
  • Bladder management
  • Change recumbency
  • Physical therapy
  • Seizure watch
167
Q

Differentials for non-infectious inflammatory neurologic disease?

A
  • Granulomatous meningoencephalitis
  • Necrotizing encephalitis
  • Generalized tremor disorder
  • Trigeminal neuritis
  • Idiopathic facial paralysis
168
Q

Do we primarily see infectious or non-infectious inflammatory disease?

A
  • Here we tend to see non-infectious
169
Q

Granulomatous meningoencephalitis pathophysiology

A
  • Inflammatory disease from granulomatous infiltration of lymphocytes, plasma cells, macrophages
170
Q

Etiology of granulomatous meningoencephalitis

A
  • Unknown

- Infectious, neoplastic, autoimmune?

171
Q

Where in the nervous system can GME affect?

A
  • Ocular (optic neuritis)
  • Focal (Brainstem/cerebellar)
  • Disseminated (cerebrum, cerebellum, brainstem, cervical spinal cord)
172
Q

Does GME primarily affect gray or white matter?

A
  • Primarily white matter

- Mass effect

173
Q

Age of dogs with GME

A
  • Young to middle aged
174
Q

Breeds with GME

A
  • Poodles and terriers
  • Small breed dogs in general
  • Peach colored miniature poodles a lot
175
Q

Clinical progression with GME

A
  • Variable
  • Acute onset
  • Progressive
176
Q

Treatment of GME

A
  • Treat with immunosuppressive drugs

- Corticosteroids, azathioprine, cyclosporine, cytosine arabinoside, procarbazine

177
Q

Prognosis of GME

A
  • Generally poor but variable
  • Survival weeks to years
  • Worst prognosis with diffuse form
178
Q

Localization:

Tetraparesis R > L

Falls/leans to the right

CP deficits in all limbs R>L

Normal spinal reflexes

Left head tilt

Positional strabismus

Horizontal nystagmus

A
  • Right central vestibular/cerebellar with paradoxical head tilt
179
Q

MRI with encephalitis

A
  • Multifocal
180
Q

Encephalitis CSF

A
  • Inflammatory

- Mononuclear (lymphocytes and macrophages), pleocytosis

181
Q

Encephalitis protocol

  • What are the four drugs, and what is the purpose of them?
A
  • TMPS (broad spectrum that crosses BBB)
  • Clindamycin (Toxoplasma and Neospora)
  • Doxycycline (Rickettsial and more bacterial coverage)
  • Prednisone (low doses)
182
Q

Encephalitis protocol once you’ve ruled out infectious organisms

A
  • D/C TMPS, Clindamycin, doxy
  • Increase prednisone dose to 2-4 mg/kg/day at high doses for several weeks and gradually taper over months depending on clinical status
  • 25% weaning over one month usually over a period of 4-6 months
  • +/- Aazathioprine, cyclosporine, Cytosine arabinoside, Procarbazine, radiation therapy
183
Q

What are the two types of necrotizing encephalitis?

A
  • Necrotizing leukoencephalitis

- Necrotizing meningoencephalitis

184
Q

Who gets necrotizing leukoencephalitis?

A
  • Primarily Yorkies

- Juveniles to young adults

185
Q

Signs with NLE?

A
  • Forebrain and brainstem signs

- WHite matter necrosis and cavitations

186
Q

Etiology of NLE

A
  • Unknown
187
Q

Prognosis of NLE

A
  • Poor

- Typically fatal within weeks to months

188
Q

Who gets necrotizing meningoencephalitis?

A
  • 1° pugs, maltese

- Juvenile to young adults

189
Q

Signs with NME

A
  • Forebrain signs and seizures

- Gray and white matter necrosis/cavitations

190
Q

Etiology of NME

A
  • Unknown
191
Q

Prognosis for NME

A
  • POOR

- Typically fatal within weeks to months

192
Q

Generalized tremor disorder - what does it look like?

A
  • Diffuse, fine, whole body tremor
193
Q

Who gets generalized tremor disorder?

A
  • Small breed dogs like maltese, Westies, Mini Pinschers

- Usually young

194
Q

CSF of generalized tremor disorder

A
  • Mild lymphocytic pleocytosis (encephalitis)
195
Q

Treatment of generalized tremor disorder

A
  • Immunosuppressive doses of prednisone
196
Q

Prognosis of generalized tremor disorder

A
  • Prognosis is good but relapse possible
197
Q

Idiopathic trigeminal neuritis**

What is the main problem?

A
  • BILATERAL mandibular branch problem with dropped jaw
  • +/- sensory branch problem
  • +/- Horner’s syndrome
198
Q

Clinical signs with idiopathic trigeminal neuritis?

A
  • Dropped jaw

- Masseter and temporalis atrophy

199
Q

Treatment of idiopathic trigeminal neuritis

A
  • Nutritional support and PT
200
Q

Prognosis of idiopathic trigeminal neuritis

A
  • Recovery of jaw function in 4-6 weeks

- Persistent muscle atrophy often

201
Q

Underlying pathophysiology of idiopathic facial paralysis

A
  • Unilateral or bilateral CN 7 palsy (neuritis)
  • Usually no other neuro deficits
  • +/- CN 8 vestibular problem
202
Q

Clinical signs of idiopathic facial paralysis

A
  • Facial paralysis

- CS max at 7 days

203
Q

Recovery of idiopathic facial paralysis

A
  • 3-6 weeks

- Some don’t fully recover

204
Q

How to diagnose idiopathic facial nerve paralysis?

A
  • Rule out inner ear disease
  • Hypothyroidism
  • Diagnosis of exclusion
205
Q

Treatment for idiopathic facial nerve paralysis?

A
  • No treatment but lubricate eyes
206
Q

Who gets idiopathic geriatric vestibular disease?

A
  • Older dogs
207
Q

Idiopathic geriatric vestibular disease signs

A
  • Acute onset of peripheral vestibular signs (CN 8 neuritis)
  • Mild head tilt to severe imbalance/rolling
  • Usually unilateral signs
208
Q

Treatment for idioapthic geriatric vestibular disease

A
  • None

- Improve rapidly, although can take 2-3 weeks for complete recovery

209
Q

Residual signs with idiopathic geriatric vestibular disease

A
  • Residual head tilt

- Can relapse

210
Q

Diagnosis of idiopathic geriatric vestibular disease

A
  • Rule out other causes of peripehral vestibular disease
211
Q

Idiopathic vestibular disease in cats

A
  • Can happen but rare

- At any age

212
Q

What is important for intracranial trauma?

A
  • Prompt recognition is essential

- Clinical history is important

213
Q

Traumatic injuries

A
  • Abrasions
  • Lacerations
  • Epistaxis
  • Otic hemorrhage
  • Oral/dental trauma
  • Eye trauma
  • Skull fractures
214
Q

Signs of shock

A
  • Alteration in mental status
  • Hypotension
  • Weak peripheral pulses
  • Tachycardia
  • Prolonged CRT
  • Pale mucous membranes
  • Hypothermia
215
Q

What must you treat first - intracranial signs or hypotensive shock?

A
  • HYPOTENSIVE SHOCK!

- DOn’t know if the changes in mental status are from shock or from the intracranial trauma

216
Q

Neurologic abnormalities that can be seen

A
  • Mental alteration
  • Depressed to coma
  • Postural deficits
  • CN deficits
  • Gait/CP deficits - be cautious assessing because may have concurrent spinal injury
217
Q

What do bilateral miotic pupils suggest?

A
  • Diffuse cerebrocortical disease
  • Lack of UMN inhibition to CN3 leading to over-firing
  • This would be with intracranial signs; if no signs, could just be bilateral ulcers
218
Q

What do unilaterally mydriatic eyes suggesT?

A
  • Unilateral caudal transtentorial herniation due to unilateral compression of CN 3
  • One is dilated and no PLR
219
Q

What do bilaterally mydriatic eyes suggest?

A
  • Bilateral caudal transtentorial herniation or foramen magnum herniation
  • Or blindness or hypertension…but IDK
220
Q

What does caudal transtentorial herniation mean?

A
  • Tissue in the occipital lobe will slide through and push on the brainstem
221
Q

WHy is herniation so concerning?

A
  • If you see signs of herniation, you worry about irreversible damage and poor prognosis
222
Q

Other clinical signs seen with intracranial trauma?

A
  • Seizures
  • Respiratory alterations (hyperventilation to apnea)
  • Cushings reflex
  • Brain-heart syndrome
223
Q

What part of the brain controls ventilation?

A
  • Brainstem

- If there’s injury, can cause hyperventilation to apnea

224
Q

Cushings reflex

A
  • Hypertension and reflex bradycardia***
  • When ICP goes up, the systemic blood pressure goes up to try and perfuse the brain better
  • Then baroreceptors of the heart slow down HR
  • Opposite of shock
225
Q

How could you differentiate intracranial trauma depression vs depression from hypovolemic shock?

A

Shock: hypotension and tachycardia

Cushings reflex: hypertension and bradycardia

226
Q

Brain-heart syndrome?

A
  • Large amount of catecholamine release –> VPCs
227
Q

Treatment for brain-heart syndrome

A
  • Lidocaine
228
Q

What are the two types of injury that can happen after trauma?

A
  • Primary and secondary injury
229
Q

Primary injury

A
  • Direct injury to brain parenchyma and blood vessels
230
Q

Secondary injury to the brain

A
  • ATP depletion
  • Ca/Na accumulation
  • Glutamate
  • Cytokines
  • Free radical
  • Lactic acid
  • Arachidonic acid
231
Q

What is the goal of treatment with brain trauma?

A
  • Minimize secondary injury
232
Q

What is the Monroe-Kelli doctrine?

A
  • three compartments within a rigid skull are brain, CSF, and blood
  • If one compartment increases, then the other compartments would have to decrease
  • If you have to decrease blood, that can lead to perfusion decreasing
  • If it’s CSF, that can cause a syrinx
233
Q

What is cerebral perfusion pressure and how is it measured?

A
  • CPP is the primary determinant of cerebral blood flow

- CPP = MABP (100) - ICP (8-12)

234
Q

Mean arterial blood pressure

A
  • 100

- Blood going to the brain

235
Q

Intracranial pressure

A

-Pressure in the brain (8-12)

236
Q

What happens to vessel tone and intracranial pressure if blood pressure goes up?

A
  • Vessels in the brain vasoconstrict

- This will decrease ICP

237
Q

What happens to vessel tone and intracranial pressure if blood pressure goes down?

A
  • Vessels in the blood vasodilate

- ICP increases

238
Q

What are the two types of autoregulation that the brain does?

A
  • Pressure

- Chemical

239
Q

What happens to vessel tone and intracranial pressure if PaCO2 goes down?

A
  • Hyperventilating

- Vessels constrict and push less blood to the brain, which lowers ICP

240
Q

What happens to vessel tone and intracranial pressure if PaCO2 goes up?

A
  • THIS IS DANGEROUS

- CO2 goes up, vessels dilate and push more blood to the brain, which increases ICP

241
Q

Emergency stabilization with brain trauma

A
  • Treat for hypovolemic shock***
  • Fluid therapy has not been proven to aggravate brain edema during hypovolemic shock
  • Repeat neurologic examinations
242
Q

What is very important in patients with intracranial trauma?

A
  • Determine oxygenation and ventilation status

- Treat hypoxemia

243
Q

How do you determine oxygenation and ventilation status?

A
  • Blood gas
244
Q

Treatment for hypoxemia

A
  • Face mask
  • Nasal oxygen catheter
  • Oxygen cage
  • Transtracheal oxygen
245
Q

What to do if a patient is hypoventilating?

A
  • Intube and mechanical ventilation
246
Q

Medical management for intracranial trauma

A
  • Mannitol
  • Hypertonic saline
  • Other
247
Q

What concentration is mannitol?

A
  • 20-25%
  • 20% is 20g/100mL
  • Calculate this
248
Q

Dose of mannitol

A
  • 1g/kg IV
249
Q

What do you give mannitol with?

A
  • 1mg/kg IV of furosemide

- Fluid therapy (1.5 maintenance)

250
Q

How to give mannitol?

A
  • Crystallizes in room temperature
  • Warm to 37°C prior to using
  • Give slowly
251
Q

MOA of mannitol?

A
  • Decreases blood viscosity –> reflex vasoconstriction –> decreases ICP (can see effect within a few minutes)
  • Osmotic diuretic (15-30 minutes)
  • Decreases CSF production
  • Free radical scavenger
252
Q

What can happen with repeated doses of mannitol?

A
  • Rebound effect if you dehydrate the patient

- More ischemic injury

253
Q

Contraindications for mannitol

A
  • DEHYDRATED or hypovolemic PATIENTS!

- They must be euhydrated

254
Q

How does hypertonic saline work?

A
  • Osmotic effect
255
Q

MOA of hypertonic saline

A
  • Osmotic effect
  • Prevents vasopsasm of damaged cerebral vessels which allows better prfusion to the brain
  • Immunomodulatory effects
256
Q

When might you give hypertonic saline over mannitol?

A
  • If you’re worried about increased ICP as well as shock

- This might be better since mannitol is contraindicated

257
Q

Dose of hypertonic saline

A
  • 5.4 mLs/kg IV bolus ove 5 minutes
258
Q

What to do concurrently with hypertonic saline?

A
  • Monitor Na level
259
Q

Why is hypertonic saline useful for shock?

A
  • resuscitation fluid, can use concurrently to treat hypovolemic shock
260
Q

Other management of patients with intracranial pressure elevations?

A
  • Head elevation to help with venous return
  • Avoid jugular compression which would decrease venous return and increase ICP
  • Monitor CO2 level for hypoventilation
  • Minimize excessive vocalization and panting
  • MOnitor HR and BP
  • Monitor PLR and size of pupils
  • Seizure watch
  • Repeat neurologic examination
261
Q

What medication should you NOT give to a patient with possible intracranial trauma?

A
  • NO corticosteroids
  • Little evidence to support usage and has increased mortality in people
  • Exacerbate/cause transient hyperglycemia due to insulin resistance –> glucose fuels anaerobic glycolysis –> lactic acidosis –> ischemic brain injury/edema –> increase in ICP

-

262
Q

What about DMSO for intracranial pressure elvations?

A
  • Questionable
263
Q

Hypothermia for ICP elevations with trauma?

A
  • Questionable
264
Q

Barbituate coma for ICP elevations with trauma?

A
  • QUESTIONABLE
265
Q

Indications fo craniotomy or craniectomy

A
  • Open skull fractures
  • Depressed skull fractures
  • FB removal
  • Hematoma removal
  • Deteriorating neurologic status despite aggressive medical therapy**
266
Q

What is required prior to surgery with trauma cases that are going downhill?

A
  • Intracranial imaging
267
Q

ICP monitoring devices

A
  • They measure ICP in real time

- Cost-prohibitive but accurate

268
Q

Principles of head trauma

A
  • Recognize!!
  • Aggressive tx
  • COntinuous monitoring
  • Repeated neuro assessment
  • Prevent further increases in ICP
  • Client education is important
269
Q

Prognosis for patients with trauma and correlation with initial neuro status?

A
  • Initial neuro status does not correlate well with clinical outcome
  • Give them 72 hours!
270
Q

Permanent neuro damage that may happen secondary to intracranial trauma?

A
  • May be permanent

- 50-75% develop a seizure disorder

271
Q

Localize:

  • Dull mentation
  • Non-ambulatory tetraparesis
  • Normal reflexes
  • Absent menace right (avisual)
  • Decreased cortical facial sensation right
  • Vertical nystagmus
  • Positional strabismus
  • Intention tremors
A
  • Left supratentorial

- Central vestibular/cerebellar

272
Q

Lead signs

A
  • Behavioral changes, tremors, seizures, ataxia, blindness, megaesophagus, laryngeal paralysis
273
Q

Strychnine signs

A
  • Sawhorse stance, erect ears, opisthotonus, seizures
274
Q

Metaldehyde signs

A
  • Sawhorse stance, erect ears, opisthotonus, seizures
275
Q

Ethylene glycol signs

A
  • Ataxia, seizures, coma
276
Q

Metoclopramide signs

A
  • Seizures
277
Q

Doxorubicin signs

A
  • Head tremors
278
Q

Ivermectin signs

A
  • Ataxia, tremors, seizures, coma (MDR1+)
279
Q

Aminoglycosides signs

A
  • Deafness, vestibular signs
280
Q

Lidocaine signs

A
  • Seizures, tremors,ataxia
281
Q

Metronidazole toxicity signs

A
  • Vestibular ataxia
  • Stiff head
  • Right head tilt
  • Leaning and listing to the right
282
Q

How does metronidazole toxicity?

A
  • Inhibits GABA release
283
Q

Dose of metronidazole that can lead to toxicity

A
  • 50 mg/kg/day

- This is higher than the dose in Plumbs

284
Q

Metronidazole toxicity signs with dogs

A
  • Vestibular

- Typically central

285
Q

Metronidazole toxicity signs with cats

A
  • Cerebral

- Blindness, seizures

286
Q

Treatment for metronidazole toxicity

A
  • Discontinue metronidazole
  • IVF
  • Diazepam can speed up recovery
287
Q

How long can recovery take with metronidazole toxicity

A
  • Takes 1-2 weeks
288
Q

What is the term for a stroke in a dog?

A
  • Cerebral vascular accident
289
Q

Vascular dfdx

A
  • Cerebral vascular accident
  • Hemorrhage or coagulopathy
  • Arteriovenous malformation
  • Feline ischemic encephalopathy
290
Q

Feline ischemic encephalopathy

  • What is it?
  • What causes it?
  • Treatment
  • Prognosis?
A
  • Ischemic necrosis of one side of the cerebrum
  • Middle cerebral artery
  • Cuterebra migration?
  • Ivermectin treatment
  • Can improve
291
Q

Do strokes happen in dogs and cats?

A
  • Yes
292
Q

CVA definition

A
  • Acute disorder of the brain resulting from cerebral ischemia or spontaneous hemorrhage
293
Q

What are the two types of stroke?

A
  • Ischemic strokes

- Hemorrhagic strokes

294
Q

WHat is more common: ischemic or hemorrhagic stroke?

A
  • 90% of the time it’s ischemic in dogs
295
Q

Causes of Ischemic strokes (thrombus formation)

A
  • Hypercoagulable states
  • vasculitis
  • Atherosclerosis
  • Parasite migration
296
Q

Causes of hemorrhagic strokes

A
  • Hypertension

- Coagulopathy

297
Q

CLinical signs of CVA

A
  • Acute onset
  • Asymmetric
  • Variable (location dependent)
  • Non-progressive after 24-48 hours
298
Q

Workup of CVA

A
  • CBC/CHem/UA/Bile acids/endocrine testing
  • Coagulation panel
  • Serial blood pressure monitoring
  • Advanced imaging like MRI, MRA
  • CSF
299
Q

On what % of cases of CVA is an underlying cause not identified?

A
  • ~40%
300
Q

What % of CVA cases have hypertension?

A
  • 40-50% CVA
301
Q

Causes of hypertension

A
  • Renal disease*
  • Hyperthyroidism
  • Hypothyroidism
  • Hyperadrenocorticism*
  • Pheochromocytoma
  • Diabetes mellitus
  • Primary?
302
Q

How can renal disease contribute to a CVA?

A
  • Hypertension

- Also through urine loss and loss of antithrombin III

303
Q

Localize:

  • Asymmetric tetraparesis L>R
  • Reduced to absent menace left (avisual)
  • Absent facial cortical sensation on the left
A
  • Right supratentorial
304
Q

Top 5 intracranial differentials?

A
  • Hydrocephalus
  • Meningitis/encephalitis
  • Tumor
  • Cerebral vascular accident (CVA)
  • Trauma
305
Q

General diagnostic tests for intracranial disease

A
  • Metabolic workup (CBC/Chem/UA/bile acids/endocrine testing)
  • Serial blood pressure
  • Advanced imaging (*MRI or CT)
  • CSF analysis, titers, cultures
  • +/- thoracic rads, abdominal ultrasound
  • +/- urine metabolic screening
306
Q

Common treatments for intracranial disease

A
  • Seizure management
  • Encephalitis protocol
  • Managing increases in ICP (mannitol, lasix, hypertonic saline)
  • Ventricular shunting and/or medications for hydrocephalus
  • Decompressive surgery - craniotomy or craniectomy
  • Tumor resection
  • Fractionated radiation therapy
  • Radiosurgery
  • Chemotherapy
  • Treating underlying metabolic disease
  • Rehabiliation

Neurology (14 decks)

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