Intracranial disease Flashcards
1
Q
Telencephalon - what is it?
A
- Cerebral cortex
2
Q
Diencephalon - what is it?
A
- Hypothalamus, thalamus, and pituitary
3
Q
Mesencephalon - what is it?
A
- Midrain
4
Q
Metencephalon - what is it?
A
- Cerebellum and brainstem
5
Q
Myelencephalon - what is it?
A
- Medulla oblongota
6
Q
Supratentorial structures
A
- Telencephalon
- Diencephalon
- CN 1-2
7
Q
Infratentorial structures
A
- Mesencephalon
- Metencephalon
- Myelencephalon
- CN 3-12
8
Q
Where is the functional cross-over?
A
- Mesencephalon
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)
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
11
Q
Which CN is contralateral infratentorial?
A
- CN IV (trochlear nerve)
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
13
Q
Characterize the cerebellar ataxia?
A
- Hypermetria ataxia
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
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)
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
17
Q
What are the two localizations of a head tilt?
A
- Cerebellar
- Vestibular
18
Q
Where does circling localize?
A
- Cerebellar
- Vestibular
- Supratentorial
19
Q
Where does positional strabismus with no resting strabismus localize?
A
- Vestibular dysfunction!
20
Q
Where do intention tremors localize?
A
- Cerebellar
21
Q
WHere does the rebound phenomenon localize?
A
- Cerebellar
22
Q
Localize:
R head tilt, falling to the R, circling to the R
A
- Right vestibular
23
Q
DAMNITV
A
- D (degenerative)
- A (anomalous)
- M (metabolic)
- N (neoplastic, nutritional)
- I (inflammatory from infection or not)
- T (trauma, toxicity
- V (vascular
24
Q
Top 5 Intracranial differentials (KNOW)
A
- Hydrocephalus
- Meningitis/encephalitis
- Tumor
- Cerebral vascular accident (CVA)
- Trauma
25
Degenerative neuro disease definition
- failure of neural elements to survive --> primary intracellular pathophysiologic defect (enzyme or something)
26
Examples of degenerative neuro diseases
- Storage diseases
- Leukodystrophy
- Neuroaxonal dystrophy
- Dysmyelination
- Cerebellar abiotrophy
- Age-related degeneration/cognitive dysfunction
27
Clinical clues to degenerative diseases
Signalment
- Age, sex, breed
| - Often weeks to months old
28
Clinical clues to degenerative diseases
Disease course
- Progressive!
29
Clinical clues to degenerative diseases
Painful or not?
- Not painful
30
Clinical clues to degenerative diseases
Localization?
- Often multifocal or widespread clinical signs
31
What degenerative diseases can lead to organomegaly?
- Storage diseases
32
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
- Supratentorial with cerebellum
33
What are two localizations for a menace deficit that is visual?
- CN VII or cerebellum
34
Describe the typical answer of each for ceroid lipofuscinosis (Batten's disease)
- Progression of clinical signs
- Pain
- MRI
- CSF
- Diagnosis
- Slowly progressive
- Non-painful
- MRI showed mild bilateral cortical atrophy, hydrocephalus
- CSF was normal
- Dagnosis: Urine metabolic screening and ultimately Histopathology
35
Anomalous differentials
- Hydrocephalus
- Hydrancephaly
- Lissencephaly
- Cerebellar hypoplasia
- Caudal occipital malformation syndrome
36
Hydrocephalus definition
- Abnormal dilation of the ventricles
37
Hydrocephalus general cause categories?
- Congenital vs acquired
38
Label the ventricles
- Just do it
39
What is most common cause of congenital hydrocephalus?
- Stenosis of the mesencephalic aqueduct
40
Breeds predisposed to congenital hydrocephalus
- Chihuahuas
- pugs
- Maltese
- Boston Terrier
- Yorkies
41
Appearance with congenital hydrocephalus
- Dome-shaped head
- Persistent fontanels (soft spot in the skull where the sutures didn't come together)
- Ventral/lateral strabismus
42
Clinical signs of congenital hydrocephalus
- Supratentorial signs usually
- Poor learners
- Behavioral changes
- Visual deficits
- Circling
- Seizures
- +/- infratentorial signs
43
Diagnosis of congenital hydrocephalus
- SIgnalment (breed)
- Clinical signs
- Imaging (U/S, CT, MRI)
- CSF analysis to rule out inflammatory disease
44
Prognosis for congenital hydrocephalus
- Extremely guarded
45
Treatment for congenital hydrocephalus
- Prednisone therapy to decrease CSF
- Diuretics (acetazolamide, mannitol, furosemide)
- Omeprazole to decrease CSF production
- Ventricular CSF shunting
46
Complications of ventricular CSF shunting
- Infections
- Undershunting or overshunting
- Mechanical failure or obstruction
47
Are all hydrocephalic dogs clinical?
- No
48
Hydrancephaly definition
- Cerebral hemisphere reduced to fluid-filled sac
| - Meninges and ependyma intact
49
What can cause hydrancephaly in kittens?
- Panleukopenia (distemper) in kittens
50
Lissencephaly definition
- Smooth brain
| - Minimal sulci/gyri
51
WHat causes lissencephaly?
- Abnormal cerebral cortical neuronal migration during fetal development
52
WHich breeds get lissencephaly?
- Lhasa apso dogs
- Wire-haired fox Terrier
- Irish Setter
- Korat cats
53
Signs of lissencephaly
- Seizures
- Poor learning
- BLindness
- Typically non-progressive
- Non-fatal
54
What is cerebellar hypoplasia?
- Abnormal development of the cerebellum
55
What can cause cerebellar hypoplasia in dogs and cats?
- Viral infection in utero or first few weeks of life
- Cats: Distemper (Parvovirus)
- Dogs: Herpesvirus? Parvovirus?
56
WHo gets developmental cerebellar hypoplasia and lissencephaly?
- Wire Haired Fox Terriers
| - Irish Setters
57
Signs of cerebellar hypoplasia?
- CSF first when tries to stand and walk
| - Non-progressive if survives systemic signs of viral infection
58
How can you tell apart cerebellar hypoplasia vs cerebellar abiotrophy?
- Cerebellar abiotrophy will get worse
| - Cerebellar hypoplasia may improve or shouldn't progress
59
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
- C1-C5 (left sided)
- Infratentorial left sided
- Supratentorial right sided
- UMN CP deficits L>R
60
Top 5 intracranial differentials again
- Hydrocephalus
- Meningitis/Encephalitis
- Vascular accident
- Tumor
- Exogenous trauma
61
Top 5 spinal dfdx
- IVDD
- Meningitis/myelitis
- Discospondylitis
- Tumor
- Exogenous trauma
62
Caudal occipital malformation syndrome name in humans
- Chiari type I malformation
63
What is caudal occipital malformation syndrome?
- Malformation of the caudal occipital area
| - Overcrowding of the caudal fossa
64
Consequences of caudal occipital malformation syndrome
- 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)
65
Diagnostic plan for suspected caudal occipital malformation syndrome?
- Advanced imaging
| - +/- CSF analysis +/- cultures and titers
66
Appearance on MRI of COMS
- 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
67
Syringohydromyelia
- CSF accumulation within the spinal cord
| - Can involve the central canal
68
Hydromyelia
- Cavity within the parenchyma not involving the central canal
- If it breaks into the central canal it's syringohydromyelia?
69
Treatment options for COMS
- Prednisone therapy
- +/- omeprazole
- +/- .l;''''''''''''']]]]],kgabapentin for pain
- Surgery
70
What surgery for treatment of COMS
- Foramen magnum decompression
71
Signalment for COMS
- Small breed dogs, specifically CKCS
| - Mean age at time of surgery 3.9 years
72
Clinical signs of COMS
- 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)
73
Why do dogs with COMS scratch?
- 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
74
Metabolic causes of neurologic disease
- Liver disease (hepatic encephalopathy)
- Renal encephalopathy
- Glucose abnormalities
- Electrolyte abnormalities (Ca, Na, K)
- Hypertriglyceridemia
- Thyroid abnormalities
- Adrenal abnormalities
75
Clinical clues to metabolic encephalopathies
- 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
76
What are the toxins with hepatic encephalopathy?
- GABA, aromatic acid, mercaptans, skatoles, ammonia
77
Pathophysiology of hepatic encephalopathy
- Toxic to white matter (oligos) --> demyelination
| - Toxic to gray matter (basal nuclei) --> ischemic neuron
78
Signs with hepatic encephalopathy in dogs
- Typically supratentorial
- Obtundation
- Abnormal behaviors
- Head-pressing
- Visual deficits
79
Signs with hepatic encephalopathy in cats
- Ptyalism
80
When can clinical signs be worse with hepatic encephalopathy?
- After eating
81
MRI with hepatic encephalopathy
- Widened sulci
| - Lentiform nuclei
82
Hypoglycemia clinical signs
- Mental alteration (dullness to coma)
- Irritability
- Pupillary dilation
- Seizures
- Tremors
- Generalized weakness
- Visual deficits
83
Glucose levels where we worry about seizures
- <30 mg/dL for sure
| - Worry at <50 mg/dL
84
Mechanisms of clinical signs with hypoglycemia
1. neuroglycopenia
| 2. Sympathetic nervous system stimulation
85
Hypernatremia pathophysiology
- 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
86
Idiogenic osmoles
- With chronicity (>2-3 ays) brain cells produce idiogenic osmoles to compensate for extracellular hyperosmolality
87
Hyponatremia pathophysiology?
- Hypoosmolality --> swelling of brain cells --> brain edema
88
What happens if you correct chronic hypernatremia too rapidly?
- Cerebral edema
89
What happens if you correct chronic hyponatremia too rapidly?
- Thalamic myelinolysis
- Brain cell dehydration
- Hemorrhage
90
What is the safe rate of correction with sodium?
- <0.5 mEq/L/hr
91
Hypothyroidism - which neurologic signs can be seen?
- 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
92
WHat is myxedematous stupor?
- Rare, life-threatening
| - Doberman Pinschers get it
93
Hyperthyroidism neurologic signs
- Restlessness, irritable, aggressive, wandering, pacing, circling
- Seizures
- Cerebral vascular accidents (hypertension)
- Muscle weakness - tremors, ventral neck flexion due to hypokalemia
94
Hyperadrenocorticism possible clinical signs
- 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
95
WHat is Nelson's syndrome?
- Acute neurologic dysfunction following adrenolytic therapy
96
Cushings Myotonia
- Failure of the muscles to relax
| - Inappropriate tone in the muscle
97
Sound of myotonic potentials on EMG
- Dive bombers
- You can hear the muscle fire
- Waxing and waning
98
Thiamine deficiency - how can it happen?
- Lack of intake (anorexic for a LONG time)
- Thiaminase (all fish diet)
- Overcooking meat
99
Which species is most affected by Thiamine deficiency?
- Cats
100
Lesions associated with thiamine deficiency
- Polioencephalomalacia
- Bilateral oculomotor, vestibular, lateral geniculate nuclei
- Caudal colliculus
- In dogs, the cerebellum and cerebral cortex can be affected
101
Clinical signs associated with thiamine deficiency
- Acute and rapidly progressive
- Lethargy
- Inappetence
- Dilated pupils
- vestibular signs
- Visual deficits
- Ventral neck flexion
- Coma
- Opisthotonus
- Death
102
Treatment of thiamine deficiency
- IV/IM/SQ thiamine hydrochloride
103
Prognosis for thiamine deficiency
- Good if treated earlier in the disease
104
Typical age of neoplasia
- >5 years of age with a median of 9
105
Most common clinical signs of neoplasia
- Seizures are the most common
| - Behavioral changes after that
106
Most common tumor in dogs and cats
- Meningiomas
107
Who gets gliomas?
- Brachycephalic breeds
108
Where are choroid plexus tumors?
- Associated with ventricle
109
Paraneoplastic syndromes associated with pituitary tumors?
- Hyperadrenocorticism
| - Acromegaly
110
Tumors that can metastasize to the brain?
- Hemangiosarcoma
- Lymphosarcoma
- Carcinomas
111
Neurologic localization:
- Dull mental status, head pressing
- Wide circles to the right
- Left menace deficit (avisual)
- Tetraparesis, L>R
- Normal spinal reflexes
- Right supratentorial
112
Diagnostic plan for a suspected tumor?
- 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
113
MRI appearance of meningiomas
- Extra-axial
- Broad-based attachment
- Contrast enhancing
114
What is the most common brain tumor in dogs and cats?
- Meningioma
115
Where do meningiomas arise from?
- Arachnoid layer between dura and pia mater
116
Behavior of meningiomas most often
- Usually histopathologically benign
| - Extraneural metastasis are rare
117
Meningiomas in cats
- Well-encapsulated, firm, easily removable
| - Can have multiple masses
118
Meningiomas in dogs
- Usually solitary, meshwork of vessels internally, intimately attached to the underlying tissue (more difficult to remove)
119
Treatment of meningiomas (medical vs surgical)
- What do they recommend here?
- Corticosteroid to decrease edema/inflammation in the brain secondary to the tumor
- Chemotherapy (hydroxyurea)
- Radiation therapy
- Surgery
- Surgery + radiation therapy**
- Surgery and hydroxyurea
120
Prognosis for meningioma in cats
- If they have surgery, often can be curative
| - 22-27 months but often die of other things
121
Prognosis for meningioma in dogs
- 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
122
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
- R sided trigeminal nerve
| - May involve all three branches (ophthalmic, maxillary, and mandibular branch)
123
WHat causes neurotropic keratitis?
- Lack of corneal sensation (CN5 ophthalmic) --> lack of reflex tears (CN7)
- Ophthalmic branch provides homeostasis and nutrition for the cornea
124
Dfdx for CN V deficits that are unilateral and severe
****TUMOR (nerve sheath tumor, lymphosarcoma, myelomonocytic leukemia)
- Infectious/granuloma --> toxoplasma, neospora
- Trauma
125
Dfdx for bilateral atrophy of the muscles of mastication
- Trigeminal neuritis that is idiopathic
126
Diagnostic plan for suspected tumor associated with CN V deficits
- CBC/Chem/UA
- Thoracic radiographs (met check)
- Brain MRI (better than CRI)
- +/- CSF
- +/- surgical biopsy
127
Appearance of nerve sheath tumor on MRI
- In the area of CNV
| - There's a special contrast
128
Treatment options for nerve sheath tumors
- Surgical resection (technically difficult, difficult to get clean margins, cosmetic consequences)
- Fractionated radiation therapy
- Radiosurgery (<2 cm)
129
Prognosis for nerve sheath tumors
- 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
What tumors tend to be at the cerebellomedullary junction?
- Meningioma
- Choroid plexus tumor
- Nerve sheath tumor (NST)
131
Pituitary macroadenoma location
- Sella or area of the pituitary
| - Takes up contrast quite well
132
What makes a pituitary macroadenoma technically a macroadenoma?
- >1 cm in height
133
Appearance of pituitary macroadenoma on MRI
- Sella or suprasellar location
- >1 cm, expands into diencephalon
- Contrast enhancing
134
Treatment for pituitary macroadenoma
- Fractionated radiation therapy (18 treatments at 2.5 Grays)
- Radiosurgery (<2 cm)
- Median survival ~1-2 years
- Transphenoidal hypophysectomy (done here)
135
What is the name for the special surgery they do here?
- Transphenoidal hypophysectomy
136
Approach for transphenoidal hypophysectomy
- They go transphenoidally through the soft palate
- Go into the basosphenoid bone
- Incise into the dura
- Usually mucinous and melt out
137
Dfdx for what looks like a hematoma on MRI?
- Hematoma
- Hemangiosarcoma
- Make sure the dog isn't anemic and no coagulopathy
138
Metastatic hemangiosarcoma - what should you do if you suspect based on appearance of MRI
- Screen the abdomen
139
Necropsy appearance of metastatic hemangiosarcoma
- Multifocal masses
| - Sometimes you'll only see the primary mass on MR
140
MAF brain biopsy
- 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
Tocagen gene therapy
- 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
Broad categories of inflammatory neuro disease?
- Infectious vs non-infectious
143
Localization of inflammatory neuro disease?
- Multifocal, diffuse nervous signs
144
Other signs associated with inflammatory neuro disease?
- Polysystemic signs including fever
- Neck pain and diffuse spinal pain
- Ocular changes!
145
What are the broad categories of infectious disease in the brain?
- Bacterial
- Viral
- Protozoal
- Fungal
- Algae
- Parasites
- Rickettsial
- Protozoal
146
Bacterial causes of meningitis/encephalitis/neuritis
- 2° to endocarditis
- Pyometra
- Foreign body
- Nasal passages
- Middle ear
147
Fungal causes of meningitis/encephalitis/neuritis
- Cryptococcosis in cats
- Blastomycoses
- Coccidiomycosis
148
Viral causes of meningitis/encephalitis/neuritis
- Distemper
- Herpes
- Parvo
- Parainfluenza
- Rabies
- FIP
- FIV
149
What should you do if an animal is neuro and doesn't have a good vax history?
- Technically should be quarantining for 7 days
150
Protozoal causes of meningitis/encephalitis/neuritis
- Toxoplasma
| - Neospora
151
Rickettsial causes of meningitis/encephalitis/neuritis
- Ehrlichia
| - RMSF (vestibular)
152
Parasitic causes of meningitis/encephalitis/neuritis
- Cuterebra
- Toxocara
- Heartworm
153
Algal causes of meningitis/encephalitis/neuritis
- Prototheca
154
What type of virus is distemper?
- Paramyxovirus?
155
What happens to the paw pads with distemper virus?
- Hyperkeratotic pads
156
Lesions and signs in younger dogs: Distemper
- Polioencephalomyelopathy
- SEizures
- Rarely survive
- Also respiratory signs
157
Lesions and signs in older dogs with Distemper
- Leukoencephalomyelopathy
- Older dogs, less severe
- Brainstem/cerebellar/vestibular signs
- May develop myoclonus
158
Myoclonus
- Rhythmic, repetitive movement of a group of muscles, present even under anesthesia
159
Localization:
CC Cluster seizures
Obtunded
- Tetraparesis L>R
- Normal reflexes
- Left menace deficit (avisual)
- Right sided supratentorial
160
Treatment for infectious meningitis
- Craniectomy, culture, lavage
- ANtibiotics
- Any drug should get into the brain with inflammation
- She picks cidal over static
161
Do you usually have to put the skull back with a craniectomy?
- No
| - Only have to put the skull back if they cross midline
162
Localization
Seizures
Depressed, dull
Nonambulatory tetraparesis
CP deficits in all four limbs
Normal reflexes
Painful neck
- SUpratentorial
| - C1-C5 because the neck is painful too (Central cord syndrome)
163
Describe the central cord syndrome again?
- Somatotropic organization
- Lesion always wrapping around more centrally because it's knocking out the thoracic limb tracts before pelvic limb tracts
164
Appearance of cryptococcus in CSF
- Non-staining haloes
165
What should you think with eosinophils in CSF?
- Think parasites
| - It's NOT NORMAL
166
Treatment for cryptococcus
- Fluconazole (antifungal drug that crosses BBB)
- Cage rest
- Bladder management
- Change recumbency
- Physical therapy
- Seizure watch
167
Differentials for non-infectious inflammatory neurologic disease?
- Granulomatous meningoencephalitis
- Necrotizing encephalitis
- Generalized tremor disorder
- Trigeminal neuritis
- Idiopathic facial paralysis
168
Do we primarily see infectious or non-infectious inflammatory disease?
- Here we tend to see non-infectious
169
Granulomatous meningoencephalitis pathophysiology
- Inflammatory disease from granulomatous infiltration of lymphocytes, plasma cells, macrophages
170
Etiology of granulomatous meningoencephalitis
- Unknown
| - Infectious, neoplastic, autoimmune?
171
Where in the nervous system can GME affect?
- Ocular (optic neuritis)
- Focal (Brainstem/cerebellar)
- Disseminated (cerebrum, cerebellum, brainstem, cervical spinal cord)
172
Does GME primarily affect gray or white matter?
- Primarily white matter
| - Mass effect
173
Age of dogs with GME
- Young to middle aged
174
Breeds with GME
- Poodles and terriers
- Small breed dogs in general
- Peach colored miniature poodles a lot
175
Clinical progression with GME
- Variable
- Acute onset
- Progressive
176
Treatment of GME
- Treat with immunosuppressive drugs
| - Corticosteroids, azathioprine, cyclosporine, cytosine arabinoside, procarbazine
177
Prognosis of GME
- Generally poor but variable
- Survival weeks to years
- Worst prognosis with diffuse form
178
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
- Right central vestibular/cerebellar with paradoxical head tilt
179
MRI with encephalitis
- Multifocal
180
Encephalitis CSF
- Inflammatory
| - Mononuclear (lymphocytes and macrophages), pleocytosis
181
Encephalitis protocol
- What are the four drugs, and what is the purpose of them?
- TMPS (broad spectrum that crosses BBB)
- Clindamycin (Toxoplasma and Neospora)
- Doxycycline (Rickettsial and more bacterial coverage)
- Prednisone (low doses)
182
Encephalitis protocol once you've ruled out infectious organisms
- 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
What are the two types of necrotizing encephalitis?
- Necrotizing leukoencephalitis
| - Necrotizing meningoencephalitis
184
Who gets necrotizing leukoencephalitis?
- Primarily Yorkies
| - Juveniles to young adults
185
Signs with NLE?
- Forebrain and brainstem signs
| - WHite matter necrosis and cavitations
186
Etiology of NLE
- Unknown
187
Prognosis of NLE
- Poor
| - Typically fatal within weeks to months
188
Who gets necrotizing meningoencephalitis?
- 1° pugs, maltese
| - Juvenile to young adults
189
Signs with NME
- Forebrain signs and seizures
| - Gray and white matter necrosis/cavitations
190
Etiology of NME
- Unknown
191
Prognosis for NME
- POOR
| - Typically fatal within weeks to months
192
Generalized tremor disorder - what does it look like?
- Diffuse, fine, whole body tremor
193
Who gets generalized tremor disorder?
- Small breed dogs like maltese, Westies, Mini Pinschers
| - Usually young
194
CSF of generalized tremor disorder
- Mild lymphocytic pleocytosis (encephalitis)
195
Treatment of generalized tremor disorder
- Immunosuppressive doses of prednisone
196
Prognosis of generalized tremor disorder
- Prognosis is good but relapse possible
197
Idiopathic trigeminal neuritis****
What is the main problem?
- BILATERAL mandibular branch problem with dropped jaw
- +/- sensory branch problem
- +/- Horner's syndrome
198
Clinical signs with idiopathic trigeminal neuritis?
- Dropped jaw
| - Masseter and temporalis atrophy
199
Treatment of idiopathic trigeminal neuritis
- Nutritional support and PT
200
Prognosis of idiopathic trigeminal neuritis
- Recovery of jaw function in 4-6 weeks
| - Persistent muscle atrophy often
201
Underlying pathophysiology of idiopathic facial paralysis
- Unilateral or bilateral CN 7 palsy (neuritis)
- Usually no other neuro deficits
- +/- CN 8 vestibular problem
202
Clinical signs of idiopathic facial paralysis
- Facial paralysis
| - CS max at 7 days
203
Recovery of idiopathic facial paralysis
- 3-6 weeks
| - Some don't fully recover
204
How to diagnose idiopathic facial nerve paralysis?
- Rule out inner ear disease
- Hypothyroidism
- Diagnosis of exclusion
205
Treatment for idiopathic facial nerve paralysis?
- No treatment but lubricate eyes
206
Who gets idiopathic geriatric vestibular disease?
- Older dogs
207
Idiopathic geriatric vestibular disease signs
- Acute onset of peripheral vestibular signs (CN 8 neuritis)
- Mild head tilt to severe imbalance/rolling
- Usually unilateral signs
208
Treatment for idioapthic geriatric vestibular disease
- None
| - Improve rapidly, although can take 2-3 weeks for complete recovery
209
Residual signs with idiopathic geriatric vestibular disease
- Residual head tilt
| - Can relapse
210
Diagnosis of idiopathic geriatric vestibular disease
- Rule out other causes of peripehral vestibular disease
211
Idiopathic vestibular disease in cats
- Can happen but rare
| - At any age
212
What is important for intracranial trauma?
- Prompt recognition is essential
| - Clinical history is important
213
Traumatic injuries
- Abrasions
- Lacerations
- Epistaxis
- Otic hemorrhage
- Oral/dental trauma
- Eye trauma
- Skull fractures
214
Signs of shock
- Alteration in mental status
- Hypotension
- Weak peripheral pulses
- Tachycardia
- Prolonged CRT
- Pale mucous membranes
- Hypothermia
215
What must you treat first - intracranial signs or hypotensive shock?
- HYPOTENSIVE SHOCK!
| - DOn't know if the changes in mental status are from shock or from the intracranial trauma
216
Neurologic abnormalities that can be seen
- Mental alteration
- Depressed to coma
- Postural deficits
- CN deficits
- Gait/CP deficits - be cautious assessing because may have concurrent spinal injury
217
What do bilateral miotic pupils suggest?
- 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
What do unilaterally mydriatic eyes suggesT?
- Unilateral caudal transtentorial herniation due to unilateral compression of CN 3
- One is dilated and no PLR
219
What do bilaterally mydriatic eyes suggest?
- Bilateral caudal transtentorial herniation or foramen magnum herniation
- Or blindness or hypertension...but IDK
220
What does caudal transtentorial herniation mean?
- Tissue in the occipital lobe will slide through and push on the brainstem
221
WHy is herniation so concerning?
- If you see signs of herniation, you worry about irreversible damage and poor prognosis
222
Other clinical signs seen with intracranial trauma?
- Seizures
- Respiratory alterations (hyperventilation to apnea)
- Cushings reflex
- Brain-heart syndrome
223
What part of the brain controls ventilation?
- Brainstem
| - If there's injury, can cause hyperventilation to apnea
224
Cushings reflex
- 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
How could you differentiate intracranial trauma depression vs depression from hypovolemic shock?
Shock: hypotension and tachycardia
Cushings reflex: hypertension and bradycardia
226
Brain-heart syndrome?
- Large amount of catecholamine release --> VPCs
227
Treatment for brain-heart syndrome
- Lidocaine
228
What are the two types of injury that can happen after trauma?
- Primary and secondary injury
229
Primary injury
- Direct injury to brain parenchyma and blood vessels
230
Secondary injury to the brain
- ATP depletion
- Ca/Na accumulation
- Glutamate
- Cytokines
- Free radical
- Lactic acid
- Arachidonic acid
231
What is the goal of treatment with brain trauma?
- Minimize secondary injury
232
What is the Monroe-Kelli doctrine?
- 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
What is cerebral perfusion pressure and how is it measured?
- CPP is the primary determinant of cerebral blood flow
| - CPP = MABP (100) - ICP (8-12)
234
Mean arterial blood pressure
- 100
| - Blood going to the brain
235
Intracranial pressure
-Pressure in the brain (8-12)
236
What happens to vessel tone and intracranial pressure if blood pressure goes up?
- Vessels in the brain vasoconstrict
| - This will decrease ICP
237
What happens to vessel tone and intracranial pressure if blood pressure goes down?
- Vessels in the blood vasodilate
| - ICP increases
238
What are the two types of autoregulation that the brain does?
- Pressure
| - Chemical
239
What happens to vessel tone and intracranial pressure if PaCO2 goes down?
- Hyperventilating
| - Vessels constrict and push less blood to the brain, which lowers ICP
240
What happens to vessel tone and intracranial pressure if PaCO2 goes up?
- THIS IS DANGEROUS
| - CO2 goes up, vessels dilate and push more blood to the brain, which increases ICP
241
Emergency stabilization with brain trauma
- Treat for hypovolemic shock***
- Fluid therapy has not been proven to aggravate brain edema during hypovolemic shock
- Repeat neurologic examinations
242
What is very important in patients with intracranial trauma?
- Determine oxygenation and ventilation status
| - Treat hypoxemia
243
How do you determine oxygenation and ventilation status?
- Blood gas
244
Treatment for hypoxemia
- Face mask
- Nasal oxygen catheter
- Oxygen cage
- Transtracheal oxygen
245
What to do if a patient is hypoventilating?
- Intube and mechanical ventilation
246
Medical management for intracranial trauma
- Mannitol
- Hypertonic saline
- Other
247
What concentration is mannitol?
- 20-25%
- 20% is 20g/100mL
- Calculate this
248
Dose of mannitol
- 1g/kg IV
249
What do you give mannitol with?
- 1mg/kg IV of furosemide
| - Fluid therapy (1.5 maintenance)
250
How to give mannitol?
- Crystallizes in room temperature
- Warm to 37°C prior to using
- Give slowly
251
MOA of mannitol?
- 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
What can happen with repeated doses of mannitol?
- Rebound effect if you dehydrate the patient
| - More ischemic injury
253
Contraindications for mannitol
- DEHYDRATED or hypovolemic PATIENTS!
| - They must be euhydrated
254
How does hypertonic saline work?
- Osmotic effect
255
MOA of hypertonic saline
- Osmotic effect
- Prevents vasopsasm of damaged cerebral vessels which allows better prfusion to the brain
- Immunomodulatory effects
256
When might you give hypertonic saline over mannitol?
- If you're worried about increased ICP as well as shock
| - This might be better since mannitol is contraindicated
257
Dose of hypertonic saline
- 5.4 mLs/kg IV bolus ove 5 minutes
258
What to do concurrently with hypertonic saline?
- Monitor Na level
259
Why is hypertonic saline useful for shock?
- resuscitation fluid, can use concurrently to treat hypovolemic shock
260
Other management of patients with intracranial pressure elevations?
- 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
What medication should you NOT give to a patient with possible intracranial trauma?
- 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
What about DMSO for intracranial pressure elvations?
- Questionable
263
Hypothermia for ICP elevations with trauma?
- Questionable
264
Barbituate coma for ICP elevations with trauma?
- QUESTIONABLE
265
Indications fo craniotomy or craniectomy
- Open skull fractures
- Depressed skull fractures
- FB removal
- Hematoma removal
- Deteriorating neurologic status despite aggressive medical therapy**
266
What is required prior to surgery with trauma cases that are going downhill?
- Intracranial imaging
267
ICP monitoring devices
- They measure ICP in real time
| - Cost-prohibitive but accurate
268
Principles of head trauma
- Recognize!!
- Aggressive tx
- COntinuous monitoring
- Repeated neuro assessment
- Prevent further increases in ICP
- Client education is important
269
Prognosis for patients with trauma and correlation with initial neuro status?
- Initial neuro status does not correlate well with clinical outcome
- Give them 72 hours!
270
Permanent neuro damage that may happen secondary to intracranial trauma?
- May be permanent
| - 50-75% develop a seizure disorder
271
Localize:
- Dull mentation
- Non-ambulatory tetraparesis
- Normal reflexes
- Absent menace right (avisual)
- Decreased cortical facial sensation right
- Vertical nystagmus
- Positional strabismus
- Intention tremors
- Left supratentorial
| - Central vestibular/cerebellar
272
Lead signs
- Behavioral changes, tremors, seizures, ataxia, blindness, megaesophagus, laryngeal paralysis
273
Strychnine signs
- Sawhorse stance, erect ears, opisthotonus, seizures
274
Metaldehyde signs
- Sawhorse stance, erect ears, opisthotonus, seizures
275
Ethylene glycol signs
- Ataxia, seizures, coma
276
Metoclopramide signs
- Seizures
277
Doxorubicin signs
- Head tremors
278
Ivermectin signs
- Ataxia, tremors, seizures, coma (MDR1+)
279
Aminoglycosides signs
- Deafness, vestibular signs
280
Lidocaine signs
- Seizures, tremors,ataxia
281
Metronidazole toxicity signs
- Vestibular ataxia
- Stiff head
- Right head tilt
- Leaning and listing to the right
282
How does metronidazole toxicity?
- Inhibits GABA release
283
Dose of metronidazole that can lead to toxicity
- 50 mg/kg/day
| - This is higher than the dose in Plumbs
284
Metronidazole toxicity signs with dogs
- Vestibular
| - Typically central
285
Metronidazole toxicity signs with cats
- Cerebral
| - Blindness, seizures
286
Treatment for metronidazole toxicity
- Discontinue metronidazole
- IVF
- Diazepam can speed up recovery
287
How long can recovery take with metronidazole toxicity
- Takes 1-2 weeks
288
What is the term for a stroke in a dog?
- Cerebral vascular accident
289
Vascular dfdx
- Cerebral vascular accident
- Hemorrhage or coagulopathy
- Arteriovenous malformation
- Feline ischemic encephalopathy
290
Feline ischemic encephalopathy
- What is it?
- What causes it?
- Treatment
- Prognosis?
- Ischemic necrosis of one side of the cerebrum
- Middle cerebral artery
- Cuterebra migration?
- Ivermectin treatment
- Can improve
291
Do strokes happen in dogs and cats?
- Yes
292
CVA definition
- Acute disorder of the brain resulting from cerebral ischemia or spontaneous hemorrhage
293
What are the two types of stroke?
- Ischemic strokes
| - Hemorrhagic strokes
294
WHat is more common: ischemic or hemorrhagic stroke?
- 90% of the time it's ischemic in dogs
295
Causes of Ischemic strokes (thrombus formation)
- Hypercoagulable states
- vasculitis
- Atherosclerosis
- Parasite migration
296
Causes of hemorrhagic strokes
- Hypertension
| - Coagulopathy
297
CLinical signs of CVA
- Acute onset
- Asymmetric
- Variable (location dependent)
- Non-progressive after 24-48 hours
298
Workup of CVA
- CBC/CHem/UA/Bile acids/endocrine testing
- Coagulation panel
- Serial blood pressure monitoring
- Advanced imaging like MRI, MRA
- CSF
299
On what % of cases of CVA is an underlying cause not identified?
- ~40%
300
What % of CVA cases have hypertension?
- 40-50% CVA
301
Causes of hypertension
- Renal disease*
- Hyperthyroidism
- Hypothyroidism
- Hyperadrenocorticism*
- Pheochromocytoma
- Diabetes mellitus
- Primary?
302
How can renal disease contribute to a CVA?
- Hypertension
| - Also through urine loss and loss of antithrombin III
303
Localize:
- Asymmetric tetraparesis L>R
- Reduced to absent menace left (avisual)
- Absent facial cortical sensation on the left
- Right supratentorial
304
Top 5 intracranial differentials?
- Hydrocephalus
- Meningitis/encephalitis
- Tumor
- Cerebral vascular accident (CVA)
- Trauma
305
General diagnostic tests for intracranial disease
- 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
Common treatments for intracranial disease
- 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
