neuro Flashcards
(54 cards)
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
