Neuro Flashcards
What are the 3 types of ataxia?
Vestibular = inner ear, CNVIII periheral (often CN 7 and horners), vestibular nuclei rostral medullar oblongata - central (often CP def, islat CN5&7 def)
proprioceptive (lesion at or caudal to midbrain, usually spinal)
cerebellar = hypermetria
What is decerbrate rigidity?
opisthotonus + rigidity extension 4 limbs =midbrain/rostarl cerebellar lesion
What is decebellate ridgitiy?
opisthotonus + rigidity extension 4 limbs with hip flexed = cerebellum
What is pleurothotonus?
head and neck deviated to one side - mid rostral brainstem, cerebral lesions
What spinal tracts are associated with the general proprioceptive pathway and UMN pathway?
General: spinocerebellar tracts (unconcisous proprioception), fasciculatus gracillus and cuneatus (CP HL and FL)
UMN pathway: reticulospinal and rubrospinal
What is the modified Frankel score?
What spinal segments are associated with the femoral n?
L4-L6
How do you grade the patellar reflex?
0 = absent
1= hypo
2= normal
3= hyper
4= clonic
What nerves to the biceps and triceps reflex test?
Biceps = musculocutaneous (C6-C8)
Triceps = radial = (C7-T2)
What nerves are responisble for withdrawal in the forelimb and hind limb?
Forelimb = dorsal thoracic, axillary, musculocutaneous, median, ulnar and radial (C6-T2)
HL = sciatic (L6-S1)
Where is the cutaneious trunci reflex relayed to?
C8-T1
What does the cross extensor test indicate?
UMN lesion on the opposite side tested
Opposite side extends during withdrawl
What are the cranial n?
1= oflactory 2 = optic, 3 = occulomotor 4= trochlear 5=trigeminal 6= abducens 7= fascial 8= auditory/vestibulocochlear 9= glossophyngeal 10= vagus 11= spinal/accesory 12= hypoglossal
on old olympus towering top a finn and German veiwed some hops
Some say marry money but my brother says big busniess make money
What CN do menace, pupillary light and palpebral test?
menace = CN 2 and 7
pupillary reflex = CN 2 and 3 (also palpebral fissure)
palpebral = CN 5 and 7
What is the pathway of the menace reflex?
CN2, optic tract, lateral genicular nucleus (thalmus/diencephalon), occiptal lobe cerebrum, cerebeullum and facial.
When can evidence of Horner’s syndrome be seen (aka what are possible areas of damage to the sympathetic tracts)?
T1-T3
C1-C5
bracial plexsus
otitis media/interna - sympathetic fibers in petrous portion of the temporal bone
What are signs of CN 3 dysfunction?
Ventrolateral strabismus; ptosis; dilated pupils; diminished to absent PLRs
Normally: Motor to extraocular muscles; parasympathetic to pupil
Test with physiologic nystagmus and PLR
What are signs of dysfucntion of CN 4?
Dorsomedial strabismus (cat); lateral deviation of retinal vein (dog)
Normal: Motor to dorsal oblique muscle
Test: Resting eyeball position (cat); fundic examination (dog)
What are signs of CN 5 dysfunction?
Masticatory muscle atrophy; dropped jaw if bilateral; decreased or absent facial/nasal sensation
Normal: Motor to muscles of mastication (mandibular); sensory to face (ophthalmic, maxillary, mandibular)
Test: Jaw tone; muscle bulk; sensation to face, cornea, and nasal mucosa
What are signs of CN 6 dysfunction?
Medial strabismus
Normal = Motor to lateral rectus and retractor bulbi
Test = Physiologic nystagmus; resting eyeball position
What is CN 7 responisble for besides facial movement?
Motor to muscles of facial expression; parasympathetic to lacrimal glands; sensory (taste) to rostral tongue
Test: Menace response; palpebral reflex; lip retraction; ear movement; Schirmer tear test
What does CN 10 do?
Sensory and motor to pharynx, larynx, and viscera
Test with Gag reflex or oculocardiac reflex
Diminished gag reflex; dysphagia; laryngeal paralysis; megaesophagus
CN 9 is also associated with gag reflex and dysphagia
What does the accessory n do?
Motor to trapezius
Test: Evaluation of muscle mass
Dysfunctional = Atrophy of trapezius
Describe the pathway for vestibular nystagmus?
CN8 → brainstem → vestibular nuclei → medial longitudinal fasciculus → abducens and oculomotor
What nerves are associatied with the palpebral reflex?
CN5 - opthalmic br (medial palpebral), maxiallary branch lateral palpebral
CN7 (palpberal br)
To evaluate mandibular br = evaluate symmetry of masseter and temporalis mm.
What does testing nasal sensation evaluate?
ipsilateral opthalmic and maxillary n innervate masal mucosa = ipsilateral trigeminal lesion
nociceptive pathway = contralateral prosencephalic lesion
Signs assoicated with proencephalon disease
Seizures; abnormal behavior; propulsive activity; depression to coma
Head turn, normal gait; propulsive circling (usually ipsilateral to lesion) or pacing; aimless wandering; head pressing; movement disorders (rare)
Postural Reactions = Contralateral deficits
Cutaneous Sensation = Contralateral (often facial/nasal) hypalgesia
Cranial Nerves = Contralateral menace deficits with normal (optic radiation and occipital cortex) or abnormal (optic chiasm, optic tracts) PLRs; facial; tongue or pharyngeal weakness (rare)
Other = Abnormalities in thirst, appetite, thermoregulation, endocrine dysfunction
Neurologic Signs That May Be Associated With Mid to Caudal Brainstem Disease
Table • 26-4 Neurologic Signs That May Be Associated With Cerebellar Disease
How does Shiff fherrington posture occur?
Disrtuption asending inhibitory axons arising from interneurons (border cells) in the dorsal border of the grey colunm of spinal seg L1 - L4
What is spinal shock?
T3-L3 lesion with LMN signs to hind limbs
What are signs associated with LMN disease?
What comprizes the lower motor neuron unit?
nerve cell body in ventral grey matter CNS
ventral nerve root
peripheral n
muscle/disease effecting neuromuscular transmission mediated by acetylcholine
What tests can be used to differentiate between junctionpathies, neuropathies and mypoathies?
creatinine kinase, aminotrasferase (AST), tensilon test, Ach receptor antibody titer, EMG, and nerve/muscle biopsies
What are differentials for diffuse/multifocal neurologic disease?
disorders myelin formation
diffuse meningitis (shaker syndrome, GME, infectious)
metabolic
dengenerative disease (lysosomal storage disease)
intoxications (mold, algae, ethylene glycol)
What are the essential components of a motor unit?
- motoneuron = cell body (located within the central nervous system, either in the cranial nerve nuclei of the brainstem or in the ventral horns of gray matter in the spinal cord) and its peripheral axon, supported by Schwann cells.
- Neuromuscular junctions.
- Myofibers innervated by the motoneuron.
What are 3 syndromes associated with neuromuscular disorders and their CS?
- Myopathic syndrome = weakness, stiff gait, tremors, atrophy or hypertrophy, muscle pain
- Motor neuropathic syndrome (classic LMN)= flaccid paralysis/esis, neurogenic atrophy, decreased reflexes, fasiculations
- Sensory neuropathic syndrome = hypalgesia/hypesthesia (decreased pain and sensation), CP deficits, decreased reflexes without muscle atrophy
List tests to diagnosis neuromuscular disorders
blood: CK, lytes, lactate, myoglobinuria (aka ammonium sulfate precipitation test), thyroid acthylcholine recptor antibody
Electomyography = peripheral n. conduction
Muscle biopsy
Nerve biopsy
Diagram of the major components of the motor unit (1 through 7) and reflex arc. A, Sensory nerve fiber. B, Dorsal root ganglion. C, Dorsal nerve root. 1, Motor neuron. 2, Ventral nerve root. 3, Spinal nerve. 4, Plexus. 5, Motor nerve fiber. 6, Neuromuscular junctions. 7, Muscle fiber
Table • 27-1 Pathoanatomic Classification of Neuromuscular Disorders
What are types of electrodiagnostic testing?
Electromyography
Nerve conduction velocity testing (motor and sensory)
Somatosensory evoked potentials (cord dorsum potentials)
Late wave analysis (F-wave and H-reflex)
Repetitive nerve stimulation
Single-fiber electromyography
Muscle and nerve biopsy
How do you diagnose masticatory myopathy?
can be made with a positive 2M-antibody titer
Can electromyography ID disorders restricted to sensory neurons?
No
What are normal and abnormal spontaneous activty on EMG?
Normal = insertional activity, miniature end-plate potential (needle positioned in proximity to NM junction), End plate spikes (complete depolarization, motor unit action potential (normal m. not completely at rest).
Abnormal = Fibs and sharps (firing single myofibers due to destablization sarcolemmal membrane), complex repetitive discharges (group of fibers firing in synchrony due to denervation), myotonic potential (congenital myotonia)
Figure 27-2 Electromyography. A, Normal baseline (“electrical silence”). B, Miniature end-plate potentials with a single end-plate spike. C, Fibrillation potentials. D, Positive sharp waves. E, Positive sharp waves and fibrillation potentials. F, Complex repetitive discharges. (Calibration: Amplitude is represented by the vertical line: 100 µV in D, and 50 µV in all other tracings. Time base is represented by the horizontal line: 10 msec in all tracings.)
Peroneal motor nerve conduction study in a normal dog (B) and a dog with a sensorimotor polyneuropathy (C), following stimulation of the peroneal nerve at the hock, stifle, and hip. Compound motor unit action potentials (M-waves) were recorded from the extensor digitalis brevis lateralis muscle (recording electrode). A, Diagram of electrode placement. B, Normal canine peroneal motor nerve conduction study. Note that latency of the M-wave increases with greater distance between stimulating and recording electrodes. Motor nerve conduction velocities calculated in this 1-year-old dog were 69 m/sec (hip to stifle) and 57 m/sec (stifle to hock). C, Abnormal canine peroneal motor nerve conduction study. Note the polyphasia, temporal dispersion, and decrease in amplitude of the M-wave when compared with B. Motor nerve conduction velocities calculated in this 6-year-old dog were slowed: 39 m/sec (hip to stifle) and 32 m/sec (stifle to hock). These abnormalities are consistent with demyelination.
Somatosensory evoked potential study in a normal dog (B) and a dog with a sensorimotor polyneuropathy (C), following stimulation of the peroneal nerve at the level of the fourth distal metatarsus (stimulus site). Somatosensory evoked potentials were recorded from the hock, stifle, hip, and L4-5 (cord dorsum potential [CDP]). Latency measurements for sensory conduction velocity determinations are represented by T1, T2, T3, and T4. A, Diagram of electrode placement. B, Normal canine somatosensory evoked potential study. Although the somatosensory evoked potentials appear to be of similar amplitude at each recording site, the sensitivity increases from hock to L4-5. Note that 1000 individual potentials (N = 1000 to right of figure) were averaged to produce these tracings. C, Abnormal canine somatosensory evoked potential study. All sensory nerve action potentials are severely reduced in amplitude, and sensory nerve conduction velocities are slowed. Dispersion of the potentials is difficult to evaluate, as potentials are barely distinguishable from background noise. Note that compared with (B), 4000 individual potentials (N = 4000) were averaged in an attempt to minimize random background noise from the time-locked electrical signal. These abnormalities are consistent with a severe sensory neuropathy.
Diagrams showing the generation of late waves after stimulation of a mixed nerve and recording from the motor point of a muscle. A, M-wave. B, F-wave. C, H-reflex.
How do you do an EMG?
most frequently used technique for electromyography involves the use of a concentric needle electrode. The central wire of the electrode (active or exploring electrode) is insulated from the surrounding cannula (reference electrode) so that the actual area being tested (between the two) is very small. A ground electrode is used to minimize extraneous “noise.”
Normal canine M-waves (left) and F-waves (right) recorded following peroneal nerve stimulation at the hock (32 superimposed individual tracings). B, Normal canine M-waves (left) and F-waves (right) recorded following peroneal nerve stimulation at the hip (32 superimposed individual tracings). Note the longer latency of the M-waves (left) and the reduced latency of the F-waves (right) when compared with (A). C, Normal canine H-waves recorded following peroneal nerve stimulation at the hip, using a low stimulus intensity (0.6 mA). Note that M-waves are not present (left). D, The same stimulation and recording sites as used in (C), after a slight increase in stimulus intensity (to 1.0 mA). M-waves now are present (left).
Repetitive nerve stimulation. A, Normal canine repetitive nerve stimulation following 1 Hz stimulation of the peroneal nerve at the hock. Note in the data table that M-wave amplitude (Peak Amp mV), area under the M-wave (Area mVms), and percentage amplitude decrement (Amp Decr %) remain constant with consecutive stimuli. B, Decremental response in a cat following 3 Hz peroneal nerve stimulation at the hock. Note that amplitude and area under the M-wave decrease with consecutive stimuli, which is measured as a percentage amplitude decrement of 17% to 44%. The cat had muscular dystrophy. C, Facilitation in a dog following 30 Hz peroneal nerve stimulation at the hock. Note that both area and amplitude of the M-wave are increased (i.e., the M-wave becomes taller and is not narrower). The increase in amplitude is represented by a negative Amp Decr %. A cause could not be determined in this dog presenting with exercise-induced weakness that occurred in warm weather. D, Pseudofacilitation in a normal dog following 30 Hz peroneal nerve stimulation at the hock. Note the increase in amplitude with no change in the area under the curve (i.e., the M-wave becomes taller and narrower). As in (C), the increase in amplitude is represented by a negative Amp Decr %.
What are the physiologic tests to evaluate the NM junction?
- Repetative nerve stimulation - repeated supramaximal while recording M waves
- Single-fiber electromyography - end plate in NM junction = v. sens for aquired myasthenia gravis
What are criteria for selection for muscle biopsy?
- Affected
- minimal approch/morbidity
- Ideally fibers oriented in 1 direction
- Previously described characteristics: latear head triceps (distal 1/3), vastus lateralus (distal 1/3), cr. tibial (prox 1/3), temporalis
- Away from tendon of insertion or aponeuroses
- Free of artifact
What are criteria for selection of nerves for biopsy?
- affected by disease, if diffuse established normal and innervates routine m. biopsy
aka: common peroneal, tibial, ulnar = all contain motor, sensory and autonomic - For sensory = cutaneous sensory n (cd cutaneous antebrachial or cd cutaneous sural)
- Nerve root biopsy
- CN biopsy - facial or trigeminal
What are the techniques for nerve biopsy?
Fascicular
full thickness
How does tissue contrast differ between T1 and T2 weighted images (short vs. long)?
T1 = short T1 relaxtion (hyperintense) - fat, long T1 relaxation (hypointense) = CSF
T2 = short T2 relaxation (hypointese) - muscle, long T2 relaxation (hyperintense) = CSF
Schematic illustrating the two basic pulse sequences, spin echo and gradient echo, and their variations. BOLD, Blood oxygenation level dependent; FIESTA, fast imaging employing steady state acquisition; FLAIR, fluid attenuation inversion recovery; FLASH, fast low-angle shot; fMRI, function magnetic resonance imaging; GRE, gradient echo; HASTE, half Fourier acquisition single-shot turbo spin echo; PDW, proton density weighted; SE, spin echo; SPGR, spoiled gradient recalled; SSFP, steady state free precession; SSFSE, single-shot fast spin echo; STIR, short-tau inversion recovery; T1W, T1-weighted; T2W, T2-weighted; true FISP, true fast imaging with steady state precession.
Substances With High Signal Intensity on T1W and T2W Images
What is the dose of water soluable iodinated contrast and gadolinium?
Water-soluble iodinated contrast medium is usually administered intravenously at a dosage of 400 to 800 mg iodine/kg
Gadolinium: intravenously at a dosage of 0.1 mmol/kg body weight = paramagnetic (enhances/strengthens the magentic field)
What is the Larmor frequency?
Spin at frequrecy porportional to the strength of the magnetic enviroment
Hounsfield Unit Measurements for Various Substances
What is the dose of contrast agents for the spine on CT?
Nonionic contrast media of choice are iohexol (Omnipaque, 240 mgI/mL) and iopamidol (Isovue, 200 mgI/mL), which are administered at dosage of 0.45 mL/kg (full spine) and 0.3 mL/kg (regional): using a cervical or lumbar puncture technique
What is the path of flow of spinal fluid?
CSF (blood ultrafiltrate) formed in Choroid plexus (lateral ventricles) → foramina 3rd ventricle → mesenchepahlic aquaduct → 4th ventricle → lateral apertures from 4th ventricle → subarachnoid space → central canal of spinal cord
What are the 3 meniginges?
pia mater
arachnoid mater
dura mater
Anatomy of spinal cord
3 meniges: dura mater (outide side), arachnoid mater, pia matter (inside)
2 spaces = subarachnoid = CSF, subdural = vessels
epidural = between bone and dura mater = fused with periosteum skull
What is in the grey mater and white matter?
Grey = neuronal cell bodies
White = axons and glial cells
Spinal cord grey on inside (outside in brain and majority of brainstem) = divides white matter into compartments (funiculi)
What is the falx cerebri?
falx cerebri = separates 2 hemispheres (connective tissue)
tentorium cerebelli = separates cerebrum from cerebellum (connective tissue)
What is the resting cell membrane potential for neurons?
Negative 80mV
Action potential = rapid depolarization by influx of Na+ through voltage gated ion channels
Iniated at axon hillock (junction between axon and neuronal cell body
all or nothing
Repolarizes by clsoure of Na channels and eflux of K through open potassium channels
Active extrusion Na in exchange for K and by K uptake by astrocytes
What is produced by oligodendrocytes?
Myelin
What is pressure autoregulation?
pressure sensative smooth m. cells maintain constant P in CNS as long as systemic BP between 50-160mmHg
Affected by intracranial disease
Graph of autoregulatory control of cerebral blood flow (CBF) and vascular diameter, in response to changes in mean arterial pressure (MAP), arterial partial pressure of oxygen (PO2), and arterial partial pressure of carbon dioxide (PCO2).
Profusion highly responsive to arterial paCO2 (as CO2 increase, profusion increase)
1mmHg change PaC02 = 5% change profusion
Intercranial disease = hypoventilation = vasodilation = increase ICP = herniation
Markedly increased profusion if PaO2 <50mmHg
What is the definition of cerebral perfusion pressure?
mean arterial pressure - intracranial pressure
How does low BP or high ICP affect cerebral profusion?
Both cause decreased cerebral perfusion pressure → ischemia in medulla → increased vasomotor tone → increase MAP → increased cerebral profusion
Hypertenion systemic → barorecptors → bradycardia
What is brain - heart syndrome?
If cerebral pressure continues to drop → increase catecholamines → myocardial ischemia → arrythmias
What is normal ICP?
8-15mmHg
ICP >15-20mmHg → abnormal, should be treated
>30mmHg significant decrease in perfusion
Durotomy decrease ICP 65% vs craniotomy alone = 15%
List drugs based on if they are good or poor at crossing the blood brain barrer.
Good = 3rd gen cephal, fluroquin, metronidazole, sulfas, chloramphenicol, trimethoprim
Mod = tetracycline, erythomycin, penicilins, rifampin
Poor = 1st and 2nd gen cepha, aminoglycocides, clindamycin, vancomyacin
What potion of the CNS is not immunologically privlaged?
meninges and choroid plexus = no BBB = normal response to inflammation (ie increased neutrophils and mononuclear cells)
What are the 2 areas in the brain where constitutive neurogenesis occurs in the adult nervous system (ie stem cells)?
subventricular zone/olfactory system
dentate gyrus of the hippocampus
What are the primary and secondary mechanisms of injury related to contusion?
1 = mechanical - swelling, hypoxia, axonal injury
2 = trauma and ischemic
- hemorrhage → decreased perfusion/energy → increase cell permability to Na, Cl, Ca
- damage → increased glutamate →increased Ca and Na uptake (via NMDA, AMPA< kainate receptors)
- increase Ca = apoptosis and activates phopholipase = increased inflammation
- increased mitochondrial permiability →free radicals → vascular damage, edema and vasospasm via increased Trpm4 and parenchyma pressure
What do micoglial (inflammatory cells) release in response to inflammation?
IL-1, TNF alpa, hydrogen peroxide, NO, proteinases
What does compression induce in the brain?
demyelination, edema, axonal degeneration and neuronal necrosis
- via physical deformation myelin (reversible) , vasogenic edema, increase glutamate = demylination via oligodendrocyte damage
Increased intracellular calcium concentration does the following: (3)
- Activates intracellular proteases such as calpains and caspase, which destroy the cytoskeleton and chromosomes and initiate programmed cell death
- Activates phospholipase A2, thereby producing eicosanoids and initiating an inflammatory response
- Binds intracellular phosphates, further depleting the cell of energy sources
What is the max amount of CSF that can be collected?
1ml per 5kg
What are the 2 locations for a CSF tap and what are the landmarks?
- Cerebellomedullary cistern: full flex skull to 90 degree with cervical spine. Intersection lines between occiptal protuberence - C2 and line along cr aspect of aspect of the wings of C2. Keep needle perpendicular to dorsal lamina.
- Lumbar cistern: Legs flexed, L5-L6 dogs, L6-L7 cats
What is considered pleocytosis for CSF (cloudy CSF)? What is a normal cell count CSF?
>500 x 10^6 WBC/L
normal = 0-5 x 10^6 WBC/L
What is a normal protein count for CSF?
<250mg/L (25mg/dL) for cerebromedullary cistern
<450mg/L (45mg/dL) for lumbar cistern
What are common serologic tests for neuro disease?
Toxo, neospora, ehrlichia, rickettsia, coccidiodies
Can do IgG index = CSF IgG/serum IgG, if low it has migrated across BBB,high then CSF is source
What is the histopathologic characteristic of DM
Necrosis primarily in lateral and ventral funiculi of TL spine
Breeds: GSD, Welsh Corgi, Boxer, Rhodesian Ridgeback
Genetic risk factor = mutation in SOD1 gene
Where do the inflammatory lesions occur for steroid responsive meninditits-artertitis (SRMA)?
Leptomeninges and associated a. - etiology unknown
Breeds: Beagle, Boxer, Berner, Weimies, NS duck trolling retrievers
Usually 6-18m range upto 7yr
What are the 3 forms of GME?
disseminated - most common
Focal - slowly progressive, suggestive of mass lesion
Ocular - pupils often fixed or dilated, optice n. swelling, chorioretinitis
What is the treatment for toxoplasma?
Clindamycin 10-25mg/kg BID 3-4 weeks
or
TMS 15mg/kg BID with pyrimethamine 1mg/kg SID
For discospondylitis, what percent are diagnosed on UA with blood culture and on direct percutaneous aspiration of the IVD?
Urine and blood culture = 40%
Percutaneous disc = 60%
What spinal segments are commonly diagnosed with FCE?
L4-L3 = 44-50%
C6-T2 = 37-42%
Where is FCE usually diagnosed?
L4-S3 = 50%
C6-T2 = 40%
What is the appearence of FCE on MRI and what percent have not lesion?
Appearence = hyperintensity on T2
21% have no lesion