Phase II Neuro Flashcards
what are the 6 components of the neurological examination
1) mentation
2) gait and posture
3) CN exam
4) postural reactions
5) spinal reflexes
6) palpation
what 2 tests do we use to assess postural reactions
1) proprioceptive tests (ex. knuckling)
2) hopping
what tests do we use to assess spinal reflexes:
- thoracic limb (TL)
- pelvic limb (PL)
- other regions
TL: withdrawal, weight-bearing
PL: withdrawal, patellar
Other regions: perianal, cutaneous trunci
what are the functional segments of the spinal cord and which are the enlargements
- C1-C5
- C6-T2 (TL enlargement)
- T3-L3
- L4-S3 (PL and perineum/tail enlargement)
what do the spinal cord enlargements contain
LMNs for the limb pairs
what lives in the white vs grey matter of the spinal cord
white matter: tracts
grey matter: motor nerve cell bodies
what are the 3(4) sections of the spinal cord white matter
- dorsal funiculus
- ventral funiculus
- lateral funiculi (left and right)
in what general area of the white matter are the ASCENDING tracts located
dorsolateral
the ascending tracts contain tracts carrying what 3 general categories of information
- conscious proprioception
- reflex proprioception
- nociception
what are the 2 conscious proprioceptive ascending tracts and which limbs do they correspond to
- fasciculus cuneatus (TL)
- fasciculus gracilis (PL)
what are the 2 reflex proprioceptive ascending tracts and what limbs do they correspond to
- rostral spinocerebellar tract (TL)
- dorsal and ventral spinocerebellar tracts (PL)
what are the 2 nociceptive tracts
- spinothalamic tract
- fasciculus proprius
what is the proprioceptive pathway
sensory receptor -> peripheral sensory neuron -> spinal cord white matter (tract) -> brainstem/cerebellum -> contralateral cortex
what ascending tracts are deepest in the white matter and what does this mean clinically
nociceptive (i.e spinothalamic and fasciculus proprius)
means that loss of deep pain is only going to be seen with a severe spinal cord injury (to the dorsolateral spinal cord)
what clinical signs would you expect to see in a patient with a lesion to the dorsolateral spinal cord (i.e. ascending tracts damaged)
1) proprioceptive deficits (decreased hopping, knuckling, proprioceptive ataxia)
2) changes in pain perception (hypoesthesia, hyperesthesia, anesthesia)
what are signs of proprioceptive ataxia
- wobble/sway
- erratic paw placement
- limbs crossing over
- abnormal posture
T/F knuckling will always indicate spinal cord dysfunction
F (pain, metabolic disease, orthopedic disease, etc.)
Are you more likely to see proprioceptive deficits (ex. knuckling) if there is a peripheral nerve or a tract problem? Why? Are both possible?
More likely in the tracts as you would need complete severage or loss of nerve fibers in the entire nerve to see proprioceptive deficits from a peripheral nerve problem. Both are technically possible (ex. severe trauma such as a car accident that severs the brachial plexus)
T/F proprioceptive ataxia is seen in both CNS and PNS lesions
F; only CNS
in what general area of the white matter are the DESCENDING tracts located
ventrolaterally
what are the 5 descending white matter tracts
- tectospinal
- rubrospinal
- vestibulospinal
- reticulospinal
- corticospinal
UMN exercises ___________ on LMN
descending inhibition (keeps reflexes in check)
where can we localize UPN to
spinal cord white matter
in what regions of the spinal cord do we tend to see ONLY UMN problems (and no LMN problems)
C1-C5 and T3-L3
LMN are confined to the _____ and localized to the (3)
PNS; spinal nerves, nerve roots or spinal cord grey matter
Describe the following for UMN:
- paralysis
- reflexes
- muscle tone
- atrophy
- urinary/GI
- clinical signs
- spastic paresis/paralysis
- normal to increased reflexes
- normal to increased muscle tone
- disuse atrophy (slow)
- incontinence
- struggling to hold body up, still have voluntary movement but it is abnormal, normal proprioception
Describe the following for LMN:
- paralysis
- reflexes
- muscle tone
- atrophy
- urinary/GI
- clinical signs
- flaccid paresis/paralysis
- decreased or absent reflexes
- decreased or absent muscle tone
- neurogenic atrophy (early and severe)
- incontinence
- cannot hold body up, no reflexes, loss of deep pain sensation
Put the following in order of increasing loss of function (and what order is gain of function)
- nociception
- proprioception
- incontinence
- paresis to paralysis
Loss of function:
1) proprioception
2) paresis to paralysis
3) incontinence
4) nociception
Gain of function occurs in the reverse order:
1) nociception
2) incontinence
3) paresis to paralysis
4) proprioception
Shiff-Sherrington posture indicates a lesion where? What are the clinical signs? Why?
- lesion in the L1-L4 grey matter border cells or their axons
- opisthotonus and increased thoracic limb extensor tone
- these neurons help co-ordinate the posture of the neck
T/F Shiff-Sherrington posture indicates poor prognosis
F: does not indicate prognosis
T/F the spinal cord and brain have no nerve endings
T
what 3 structures are involved in EXTREME spinal pain
bones, nerve roots, meninges
what do you NOT want to do to assess neck pain if other signs are present
vertical/horizontal flexion
what is a nerve root signature
single limb lameness (pain) due to nerve damage
what do you see in addition to spinal pain in a patient with concurrent spinal cord disease
paresis and ataxia -> proprioceptive deficits
As a lesion moves CRANIALLY in the spinal cord, what happens to proprioceptive ataxia in the thoracic limbs?
gets worse
what are the 3 meninges from OUTSIDE to INSIDE
dura mater, arachnoid mater, pia mater
the patellar reflex tests the function of what nerve
femoral nn
what are the spinal cord segments tested by the femoral nerve and which is the main one
L4, L5, L6
L5 is the main one
the flexor reflex tests what nerves
radial (thoracic) and sciatic (pelvic)
what spinal cord segments are tested by the flexor reflex and what is the main one
Radial:
C7, C8, T1, T2
Pelvic:
L6, L7, S1, S2
L7 is the main one
where does cutaneous trunci synapse
C8-T1
the absence of cutaneous trunci reflexes on one side only tells us
there is an impaired transmission of sensory signals that synapse between C8-T1 on that side
which is left and which is right:
OS
OD
OS: left
OD: right
what are 4 clinical signs of Horner’s syndrome and which is the MINIMAL clinical sign
- miosis (minimal clinical sign)
- enopthalmos
- protruding nictitans
- ptosis
what is the pathway of Horner’s syndrome (normal pathway)
hypothalamus -> travels in spinal cord to T1/T2/T3 -> enters sympathetic trunk -> synapses in superficial cervical ganglion -> mediates dilation of the eye
where are the synapses along the pathway for Horner’s syndrome
1) at T1/T2/T3
2) at the superficial cervical ganglion
what are the sections of the CNS
thalamocortex, brainstem, cerebellum, spinal cord
what are the sections of the PNS
peripheral nerves, neuromuscular junctions, skeletal muscles
what are the 2 types of LMNs
those leaving the cervicothoracic and lumbosacral enlargements and the cranial nerve motor neurons/ganglia
the perineal reflex tests what nerve? what segments?
pudendal (S1, S2, S3)
T/F neuromuscular disease involves lesions of both the UMN and LMN
F; it involves the LMN since neuromuscular disease involves the PNS
T/F cranial nerves may be impacted by neuromuscular disease
T, since they are considered LMNs
what is the difference between mononeuropathies and polyneuropathies
mononeuropathies: one nerve or a group of adjacent nerves affected
polyneuropathies: simultaneous malfunction of many peripheral nerves
how do neuromuscular diseases present (signs on the neurologic exam)
Presents like LMN disease
- normal mentation
- CN may be afffected
- paresis/paralysis
- decreased to absent reflexes
- decreased to absent muscle tone
- possible neurogenic atrophy
- possible paresthesia
- expect normal postural reactions unless there is concurrent sensory dysfunction
where is the cauda equina located
over the lumbosacral junction (with species differences)
T/F the cauda equina is part of the spinal cord
F, part of the PNS (LMN)
what are clinical signs of cauda equina lesions
- NO ataxia
- may see lumbosacral pain
- may see abnormal spinal reflexes
put the following species in order of shortest to longest spinal cord (i.e which ends before the lumbosacral junction and which extends the furthest past the junction)
- dog
- cat
- horse
- cow
dog, cow, horse, cat
what is a telltale sign that a lesion affecting all 4 legs is in the PNS as opposed to the CNS
lack of proprioceptive ataxia
PNS dysfunctions are characterized by
RAT
- reflex deficits
- atrophy (neurogenic)
- tone decreased
PNS dysfunctions can be a manifestation of (3)
neuropathy, junctionopathy, myopathy
T/F ataxia is uncommon with PNS lesions
T
what 3 “opathies” are clinically indistinguishable
polyneuropathies, polymyopathies and junctionopathies
describe the expected findings on the neurologic exam for a patient with neuromuscular disease:
- mentation
- cranial nerves
- posture/gait
- postural reactions
- reflexes
- muscle tone
- muscle atrophy
- other comorbidities
- mentation: normal
- cranial nerves: may be affected
- posture/gait: paresis/paralysis
- postural reactions: normal
- reflexes: reduced to normal
- muscle tone: decreased to absent
- muscle atrophy: possible
- other comorbidities: megaesophagus, aspiration pneumonia, exposure keratitis
what are important differential diagnoses for a patient showing signs of neuromuscular disease
- orthopaedic (pain)
- systemic illness (malaise)
- lumbosacral disease
are presynaptic or postsynaptic neuromuscular diseases associated with SLUDGEM
post-synaptic
what are examples of myopathies
non-inflammatory (acquired, degenerative/inherited, nutritional) and inflammatory (infectious and immune-mediated)
what 4 ways can we diagnose myopathies
- CBC/biochem/UA: elevated CK, ALT, AST
- serum pre and post-exercise lactate
- electrodiagnostics
- muscle histopathology
how do the clinical signs of hypokalemia differ between cats and dogs and why
cats: high shoulders and low head carriage
won’t see low head carriage in dogs as they have a more complete nuchal ligament
what is another word for thalamus
diencephalon
what two regions of the brain control mental status and why is this useful
the thalamocortex and the RAS in the brainstem
useful because if we see altered mental status we automatically know the lesion is in the brain
what is the order of mental status from most to least response to stimuli
alert - depressed - stuporous - comatose
what are clinical signs consistent with depressed mentation
drowsiness, inattention, decreased response to environmental stimuli
depressed mentation indicates a lesion in:
brainstem (ARAS) or thalamocortex
what are clinical signs consistent with stuporous mentation
unconscious, decreased response to external stimuli, still arousable with a painful stimulus
stuporous mentation indicates a lesion in:
brainstem (ARAS) - there is a partial disconnection
what are clinical signs consistent with comatose mentation
unconscious, no response to any external stimuli
comatose mentation indicates a lesion in
brainstem (total disconnect of ARAS)
a disoriented mentation indicates a lesion in:
thalamocortex or vestibular system
what cranial nerves nuclei live in the:
thalamus
CN II
what cranial nerves nuclei live in the:
midbrain
CN III, CN IV
what cranial nerves nuclei live in the:
pons
CN Vm
what cranial nerves nuclei live in the:
medulla
CN Vs, CN VI -> CN XII
how can we simplify the division of the CN nuclei in the brain
CN II in the thalamocortex, CN III -> XII in the brainstem
what is the pathway of the menace response
CN II (ipsilateral) -> thalamocortex (contralateral) -> cerebellum (ipsilateral) -> CN VII (ipsilateral)
what is the pathway of the PLR
CN II in -> thalamus -> midbrain (brainstem) -> CN III out
what CN are involved in physiological nystagmus
CN III, IV, VI, VIII
what is the role of the MLF
connects CN III, IV, VI, VIII in the midbrain
describe the pathway of physiological nystagmus
inner ear receptors sense movement -> info travels down CN VIII to the brainstem (vestibular nuclei) -> info travels through the MLF to CN III, IV, VI -> info carried to the left and right eyes
what is the pathway of the palpebral reflex
CN V -> brainstem -> CN VII out
what is the pathway of nasal septum stimulation
CN V -> brainstem -> cerebral cortex
masticatory and temporal muscles are innervated by
CN V (motor)
facial symmetry of ears, nose and lips is controlled by
CN VII (facial)
laryngeal function is controlled by
CN IX, CN X
tongue function is controlled by
hypoglossal (CN XII)
what section of the neurological exam does lesions in the thalamocortex not involve
spinal reflexes (only in the spinal cord, does not go to the brain)
what mentation might we see in a patient with a thalamocortical lesion
- depressed
- delirium/disorientation
- behavioural changes
why might we see proprioceptive deficits with an almost normal gait in a dog with a thalamocortical lesion
because most of movement is controlled by the brainstem (thalamocortex just responsible for voluntary movement)
what types of signs might we see in a patient with a thalamocortical lesion
- changes in mentation (depressed, delirium, disorientation)
- wandering, pacing, head pressing
- head and body turn (ipsilateral)
- mild hemiparesis (contralateral)
- circling (ipsilateral)
what CN tests would we expect to be altered in a patient with a thalamocortical lesion
- menace response (contralateral)
- nasal septum sensation deficit (contralateral)
what clinical sign is a dead giveaway that a lesion is in the thalamocortex and how do we interpret it
seizures: lesion is contralateral to side of seizures
T/F neck pain is possible in a patient with a thalamocortical lesion
T
how do we differentiate a thalamocortical from a vestibular lesion
both will have circling (ipsilateral) but only vestibular will have a head TILT (ipsilateral) as well as other vestibular signs (ex. nystagmus)
what are focal seizures
abnormal activity in one region of a cerebral hemisphere
what is a generalized seizure
abnormal activity in both cerebral hemispheres
what is usually impaired with generalized seizures
consciousness
what part of the neurologic exam would we not see any changes in a brainstem lesion
spinal reflexes (same reason as the thalamocortex)
what mentation might we expect to see in a patient with a brainstem lesion
depression, stupor, coma
does decerebrate or decerebellate rigidity have a better prognosis
decerebellate
decerebrate rigidity indicates a lesion in ______________ whereas decerebellate rigidity indicates a lesion in _______________
rostral midbrain (brainstem); cerebellar peduncles or rostral cerebellum
with a brainstem lesion, we might expect to see deficits in what cranial nerves
CN III - XII
how would postural reactions be altered in the case of a brainstem lesion
ipsilateral deficits and abnormal gait (since much of movement is controlled by the brainstem with only voluntary movement coming from the thalamocortex)
how do clinical signs differ depending on if there is a bilateral or unilateral CN Vm deficit
bilateral: dropped jaw
unilateral: atrophy of masticatory mm on that side
what are 2 signs of lesions to CN III, IV, or VI
1) strabismus
2) abnormal PLR (dilated eye) -> CN III deficit
what is unique about the pathway of CN VII
passes close to the middle/inner ear -> can be impacted by disease in the middle/inner ear
ex. with an inner ear infection you might be changes in the palpebral reflex as well as facial paralysis/asymmetry
how can we differentiate if CN VII lesions are in the CNS or PNS
CNS: will see changes in mentation, changes in other CNs, proprioceptive deficits, tetraparesis (UMN)
what causes facial spasm? how can we differentiate from fibrosis
hyperactivity in CN VII; if fibrosis, absent palpebral reflex (whereas if hyperactivity of CN VII would still see a palpebral reflex)
what components make up the vestibular system:
- PNS
- CNS
PNS:
- inner ear receptors
- CN VIII
CNS:
- vestibular nuclei (brainstem)
- cerebellum
what are the 5 outputs of the vestibular system
1) extraocular mm. via the MLF and vestibulomesencephalic tract
2) skeletal mm. via the MLF and vestibulospinal tract
3) vestibulocerebellum via the vestibulocerebellar tract
4) vomiting center via reticular formation
5) somatosensory cortex via internal capsule and medial geniculate bodies
what are the 3 types of pathological nystagmus
vertical, horizontal, rotatory
note: can also change directions with different head positions
the fast phase of nystagmus is usually (towards/away) from the side of the lesion
away
T/F CN VII originates from the brainstem and travels with CN VIII at the level of the inner ear
T
why might you see Horner’s syndrome in a patient with peripheral vestibular disease
the pathway of Horner’s syndrome travels and synapses in the superficial cervical ganglion, which is in the inner ear
this makes it susceptible to deficits if there is peripheral vestibular disease originating in the inner ear
what type of nystagmus is observed with a CNS lesion and what with a PNS lesion
CNS: horizontal, vertical, rotatory or changing
PNS: horizontal or rotatory
what makes diagnosing bilateral vestibular lesions difficult
no head tilt or nystagmus, only signs are wide based stance with bilateral ataxia and wide head excursions (side-side)
why do we see head tilt opposide to the lesion with paradoxical vestibular lesions
the cerebellum is doing too much -> moves head tilt away from lesion
