neuro Flashcards
approach to solving neurological problems
-first full physical exam and history
-neuro exam: describe abnormalities
-localize the lesion
-characterize the onset and progression: preacute, acute, chronic
-generate differential list: * LOCALIZATION, SIGNALMENT, ONSET, PROGRESSION
* TAKE A GOOD CLIENT/PATIENT HISTORY!
- USE ANCILLARY TESTS TO MAKE DIAGNOSIS
- IDENTIFY ANY CONCURRENT SYSTEMIC/METABOLIC, INFLAMMATORY OR NEOPLASTIC DISEASE
- NEURO SYSTEM TESTING
neurological exam
- A CORRECT LOCALIZATION AND DIAGNOSIS STEMS FROM A COMPLETE AND
ACCURATE NEUROLOGICAL ASSESSMENT - REQUIRES PRACTICE AND A COOPERATIVE PATIENT (AND HANDLER)
- THIS IS NOT A ONE-PERSON TASK!
6 components of neuro exam
- COMPONENTS OF THE EXAM:
1. MENTATION (anxious, dull, retunded, stuperous) want QRR
2. GAIT & POSTURE (normal prop, lameness, pyretic, ataxic)
3. CRANIAL NERVES (any deficits in CN exam)
4. PROPRIOCEPTION (does the animal know where its body is in space)
5. SPINAL REFLEXES, MUSCLE TONE & MUSCLE SIZE (atrophy/asymmetry, withdrawal reflex, perineal, cutanous trunki)
6. SENSATION & PAIN (can the animal feel)
PROPRIOCEPTION
- ABILITY TO SENSE WHERE THE LIMBS ARE IN SPACE
- EVEN MINOR DAMAGE TO ASCENDING PROPRIOCEPTIVE TRACTS (SUPERFICIAL IN CORD AND BRAINSTEM) RESULTS IN LOSS OF
PROPRIOCEPTION (ATAXIA, ABNORMAL KNUCKLING AND HOPPING) IN LIMBS CAUDAL TO LESION
upper vs lower motor neuron
LMN: neuron connecting the
CNS to the muscle
-short choppy gate, crouched
-decreased spinal reflexes
-large, easily expressed bladder, urinary incontinence
-rapid muscle atrophy
UMN: originates in brain and
controls the LMN
-long strided posture, ataxia
-normal to exaggerated spinal reflexes
-increased muscle tone
-MOSTLY INHIBITORY, so damage leads to a decrease in inhibition so you get an increase in reflexes ect.
-hard to express bladder
-slow muscle atrophy
upper motor neurons
- CELL BODIES ORIGINATE IN
CEREBRUM AND BRAINSTEM - CONNECTED TO LMNS BY
“LONG TRACTS” OR “SPINAL
PATHWAYS” - CONTROL THE LMN
- INITIATE / CONTROL MOVEMENT
- REGULATE NORMAL EXTENSOR TONE
-damage to the UMN shows UMN signs CAUDAL TO THE LESIONS
upper motor neuron signs
** IN ALL LIMBS CAUDAL TO THE LESION
* LOSS OF PROPRIOCEPTION, ATAXIA
* DECREASED MOTOR FUNCTION: PARESIS/PARALYSIS
* INCREASED EXTENSOR MUSCLE TONE
* INCREASED REFLEXES*
* GAIT: BASEWIDE STANCE, EXCESSIVE LIMB ABDUCTION WHEN
TURNING, DELAYED LIMB PROTRACTION (SLOW STEPS), LONG
STRIDES
spinal tracts cross midline rostral to brainstem so lesions are:
- LESIONS OF SPINAL CORD CAUSE
UMN SIGNS IN IPSILATERAL LIMBS
CAUDAL TO LESION - LESIONS OF BRAINSTEM CAUSE
UMN SIGNS IN IPSILATERAL LIMBS - LESIONS OF CEREBRAL CORTEX
CAUSE DEFICITS IN
CONTRALATERAL LIMBS
R sided brain lesions, contralateral brain lesions.
damage to LMN will cause lesion
-Damage to any component of the LMN causes LMN signs in the
muscles/limbs directly supplied by that LMN – AT THE LEVEL OF THE
LESION
-decreased tone, RAPID ATROPHY of muscle, weak gait.
spinal cord segment C6-T2
-* BRACHIAL PLEXUS
* FORELIMB MUSCLES
-for thoracic limb withdrawl reflex
SPINAL SEGMENT L4/5/6
- FEMORAL NERVE,
QUADRICEPS MUSCLE,
PATELLAR REFLEx
SPINAL SEGMENT L6-S2
- SCIATIC NERVE, FLEXOR
MUSCLES OF THE REAR LIMB,
WITHDRAWAL REFLEX
-sciatic reflex
SPINAL SEGMENT 1-S3
- ANUS, BLADDER
-perineal reflex S1-S3
C1 – C5 LESION
- MENTATION:
- NORMAL
- GAIT / POSTURE:
- AMBULATORY VS. NON-AMBULATORY
- TETRAPARESIS VS. TETRAPLEGIA
- +/- PROPRIOCEPTIVE ATAXIA
- PROPRIOCEPTION:
- +/- PROPRIOCEPTIVE DEFICITS X 4
- REFLEXES:
- INTACT (OR INCREASED) X 4
- TONE:
- NORMAL TO INCREASED X 4
C6 – T2 LESION
- MENTATION:
- NORMAL
- GAIT / POSTURE:
- “TWO ENGINE GAIT”
- AMBULATORY VS. NON-AMBULATORY
- TETRAPARESIS VS. TETRAPLEGIA
- +/- PROPRIOCEPTIVE ATAXIA
- PROPRIOCEPTION:
- +/- PROPRIOCEPTIVE DEFICITS X 4
- REFLEXES:
- THORACIC LIMBS – DECREASED; PELVIC LIMBS – NORMAL TO
INCREASED - TONE:
- THORACIC LIMBS – DECREASED; PELVIC LIMBS – NORMAL TO
INCREASED
T3 – L3 LESION
- MENTATION:
- NORMAL
- GAIT / POSTURE:
- AMBULATORY VS. NON-AMBULATORY
- PARAPARESIS VS. PARAPLEGIA
- +/- PROPRIOCEPTIVE ATAXIA
- PROPRIOCEPTION:
- +/- PROPRIOCEPTIVE DEFICITS X 2
- REFLEXES:
- THORACIC LIMBS – NORMAL; PELVIC LIMBS – NORMAL TO
INCREASED - TONE:
- THORACIC LIMBS – NORMAL; PELVIC LIMBS – NORMAL TO
INCREASED
L4 – S3 LESION:
- MENTATION:
- NORMAL
- GAIT / POSTURE:
- AMBULATORY VS. NON-AMBULATORY
- PARAPARESIS VS. PARAPLEGIA
- +/- PROPRIOCEPTIVE ATAXIA
- PROPRIOCEPTION:
- +/- PROPRIOCEPTIVE DEFICITS X 2
- REFLEXES:
- THORACIC LIMBS – NORMAL; PELVIC LIMBS – NORMAL TO
DECREASED - TONE:
- THORACIC LIMBS – NORMAL; PELVIC LIMBS – NORMAL TO
DECREASED
mentation
-bar or qar
-dull/ depressed (still responsive, look tired)
-obtended (mentally inapropriote but still able to be roused)
-stupourous (have to use very noxious stimulus to get response)
-coma
-behaviour changes
posture
-head tilt
-falling
-head turn
-broad base UMN)
-narrow based (LMN)
-paligrade-parasis LMN
-increased tone (UMN/cerebellar)
-decreased tone LMN
ipilateral vesibular posture signs
-head tilt
-falling
-head turn
3 types ataxia
-PATHWAYS RELAYING SENSORY INFO TO THE BRAIN OR THE BRAIN
REGULATORY CENTERS HAVE BEEN DISRUPTED AND THERE IS LOSS OF
REGULATION OF MOVEMENT
- SC/BRAINSTEM/PERIPHERAL: PROPRIOCEPTIVE LOSS ATAXIA
- VESTIBULAR: LOSS OF BALANCE
- CEREBELLUM: LOSS OF FINE MOTOR CONTROL / HYPERMETRI
LMN gaits
-weak gait, short, more flaccid, decreased gate
- WEAKNESS, PARESIS, EXERCISE INTOLERANCE
* SHORT STRIDED, MAINTAINS FEET UNDER CENTER OF GRAVITY
* MAY BE PLANTIGRADE
* MUSCLE ATROPHY*
* LOSS OF REFLEXES*
Damage to the LMN:
Spinal cord grey matter
Ventral nerve roots
Peripheral nerves
how to differentiate between muscle disease or LMN disease
animals with muscle disease have:
* Normal reflexes
* No proprioceptive deficits
(no ataxia)
* Muscle pain (common)
-less atrophy with muscle disease
ataxia/ incoordination indicates lesions to?
Spinal cord UMN “long tracts”
or
Vestibular system
or
Cerebellum
UMN “SPINAL CORD/PROPRIOCEPTIVE” ATAXIA gate
- Long, spastic stride
- Increased muscle tone
- Delay in onset of swing phase
- Disruption of
proprioceptive (sensory) ascending tracts - Abnormal postural reactions (knuckling,
hopping) Decreased proprioception
don’t know where there body is in space.
-Increased extensor muscle tone (UMN)
-Normal to increased reflexes
VESTIBULAR ATAXIA:
- LOSS OF BALANCE
- HEAD TILT, NYSTAGMUS
- PROPRIOCEPTION NORMAL** IF
PERIPHERAL VESTIBULAR (PERIPHERAL
NERVE) - PROPRIOCEPTION SLOW OR ABSENT IF
BRAINSTEM IS INVOLVED (CENTRAL
VESTIBULAR)
cerebellar ataxia
- HYPERMETRIA (LOSS OF FINE TUNING)
-Wide based stance
-Truncal swaying
-Normal strength
-Normal proprioception
-Goose-stepping
-Intention tremor
POSTURAL REACTIONS
- ABNORMAL WITH UMN LESIONS IN SPINAL CORD, BRAINSTEM +/- CEREBRAL CORTEX
- LMN LESIONS DO NOT USUALLY AFFECT CP TESTS UNLESS THERE IS SEVERE SENSORY LOSS OR LOSS OF
VOLUNTARY MOTION - USED TO DECIDE IF EACH LIMB IS NEUROLOGICALLY NORMAL OR ABNORMAL. THEN USE REFLEXES TO
CONFIRM UMN VS. LMN
spinal reflexes grading
GRADE +2 = NORMAL
* GRADE +1 = DIMINISHED
* GRADE 0 = ABSENT
* GRADE +3 = INCREASED
- NORMAL TO INCREASED (+2 TO +3)
REFLEXES IN PATIENTS WITH UMN
DISEASE - DECREASED (0 TO +1) IN LMN
patellar reflex
- FEMORAL NERVE: L4 – L6 SPINAL CORD SEGMENTS
- INCREASED WITH LESION BETWEEN
BRAIN AND L4 – L6 - DECREASED WITH LESION OF L4 – L6
SPINAL CORD SEGMENTS, NERVE
ROOTS & FEMORAL NERVE
pelvic limb withdrawl reflex
sciatic nerve L6-S2
-ability to withdrawl
-Normal to increased: Lesion cranial to L6
-Decreased: Lesion of L6-S2 spinal cord segments, nerve roots, sciatic
nerve
thoracic limb withdrawl
-C6-T2 Spinal Cord Segments
-Decreased (LMN) Brachial
Plexus injury C6-T2 Spinal
cord
-Normal to increased (UMN)
SC Lesion above C6
menance
- Sensory: CN II
- Motor: CN VII
Palpebral / corneal
- Sensory: CN V
- Motor: CN VII
- PLR (direct/consensual
- Sensory: CN II
- Motor: CN III
- Facial sensation
– CN V, CN VII
strabismus
– CN III, IV, VI
gag reflex nerves
– CN IX, X, XII
CN 2: optic nerves
- Blind
- Loss of Menace
- Loss of PLR
CN 3: OCCULOMOTOR
- Dilated Pupil
- Loss of PLR
CN 5: TRIGEMINAL
- Decreased jaw tone
- Atrophy muscles of mastication
- Loss of facial sensation
-Absent facial sensation, bilateral
-Atrophy on R side Trigeminal nerve tumor
-dropped jaw
CN 7: FACIAL
- Drooped face
- Loss of blink
- Loss of lip twitch, ear twitch
- Decreased tear production
CN 8: VESTIBULOCOCHLEAR
- Loss of Balance
- Head tilt
- Loss of Hearing
CN 9 : GLOSSOPHARYNGEAL
CN 10: VAGUS
- Dysphagia
- Loss of Gag reflex
- Laryngeal paralysis
CN 12: HYPOGLOSSAL
- Loss of tongue strength
- Tongue atrophy
- Tongue deviation
horners syndrome
-loss of SNS input to eye
-mitotic pupil, 3rd eyelid prolapsed, ptosis, enophthalamus
Peripheral vasodilation on side of lesion (ear, nose, neck) horses SWEAT!
CEREBRAL CORTEX / FOREBRAIN signs
- Seizures
- Altered behavior/mentation
- Cortical blindness (opposite)
- Diminished facial sensation
(opposite) - May circle/pace towards lesion
- Inconsistent/mild loss of CP on side
opposite lesion - Gait may be normal
- Hemi-neglect (hypoalgesia /
blindness)
brainstem lesions
- ALTERED MENTAL STATE: DEPRESSION, STUPOR, COMA
- IPSILATERAL PROPRIOCEPTIVE ATAXIA, UMN HEMIPARESIS
- MULTIPLE CRANIAL NERVE DEFICITS
- +/- VESTIBULAR SIGN
vesicular system lesion signs
- Head tilt
- Balance problems
- Vestibular Ataxia
- Nystagmus
- Proprioceptive ataxia if brainstem
(central) disease
vesibular disease central and peripheral
- HEAD TILT TOWARDS LESION
- SPONTANEOUS NYSTAGMUS AT REST (FAST PHASE AWAY FROM SIDE OF LESION):HORIZONTAL OR ROTARY
- NYSTAGMUS MAY GET WORSE OR ONLY BE APPARENT
WITH CHANGES IN BODY POSITION (POSITIONAL
NYSTAGMUS) - VOMITING, MOTION SICKNESS
peripheral vesibular disease
- NYSTAGMUS IS ALWAYS HORIZONTAL OR ROTARY AND DOES NOT CHANGE
DIRECTION AS CHANGE HEAD POSITION - POSTURAL REACTIONS AND PROPRIOCEPTION ARE ALWAYS NORMAL
- OTHER CRANIAL NERVES ARE NOT AFFECTED
- EXCEPT MAY SEE CONCURRENT HORNER’S AND/OR CN7 PARALYSIS IF
MIDDLE/INNER EAR DISEASE
central vestibular disease
- VERTICAL NYSTAGMUS
- NYSTAGMUS THAT CHANGES DIRECTION AS CHANGE HEAD POSITION
- ABNORMAL POSTURAL REACTIONS / PROPRIOCEPTION ON SAME SIDE AS
LESION - OTHER CRANIAL NERVES (BESIDES 7) AFFECTED
cerebellar disease lesions
- MENTALLY NORMAL
- STRONG, HYPERMETRIC
- EXAGGERATED LIMB RESPONSES, GOOSE STEPPING
- LOSS OF FINE TUNING OF MOTOR CONTROL
- MAY SEE HEAD TREMOR, INTENTION TREMOR
PARADOXICAL VESTIBULAR DISEASE:
- Cerebellar vestibular nuclei normally inhibit brainstem vestibular nuclei
- Cerebellar lesion will decrease normal inhibition of adjacent brainstem vestibular
nuclei - Normal brainstem side will therefore have less activity than other side
- Head tilt develops towards normal side (opposite to the side of lesion
RECOGNIZE WHEN:
-Head tilt to one side
-Postural reaction deficits + other CN deficits on opposite side (due to brainstem lesion)
-Lesion is on the side with postural reaction deficits and CN deficits (side opposite head tilt
