2.7 Principles of Brainstem Disease Flashcards

1
Q

What does the brainstem consist of?

A

the midbrain, the pons, and the medulla

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2
Q

Summary: what is the most important information to know about the brainstem?

A
  • consists of the midbrain, pons, and medulla oblongatta (reticular formation in MO)
  • has a major role in basic functions such as arousal, CVRS function, and gait generation
  • contains the nuclei of CNIII-CNXII (I and II located in forebrain)
  • brainstem disease is associated with neurological signs such as CN deficits, marked mentation changes, decerebrate rigidity, paresis, and proprioceptive ataxia (+/- vestibular ataxia)
  • use 5 finger rule (and graph) to select most-likely etiology
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3
Q

What is the function of the brainstem?

A
  • it is the major highway for all of the sensory and motor information
  • it maintains consciousness (ARAS), generates gait, vomiting reflex (CRTZ), CVRS function (ARAS), crainial nerve function (CNIII-XII: CNI and CNII are cerebral), coordination and balance
  • brainstem pathways are IPSILATERAL
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4
Q

What structures arise in the midbrian, pons, MO (and RF)

A
  • midbrain (mesencephalon): red nucleus (gait), CNIII, CNIV
  • pons (metencephalon): CNV, pontine retucular formation (gait)
  • medulla oblongatta (myelencephalon): CNVI-XII, medullary reticular formation (gait)

NOTE: the reticular formation (of the MO) is a meshwork of neuronal cell bodies regulating mental status, ARAS, sleep/wake, resp/cardio, excretion, swallowing, vomiting, and voluntary movement (gait)

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5
Q

What are the clinical signs of brainstem disease?

A
  • reduced mentation (obtunded, stuporous, comatose)
  • head tilt, decerebrate rigidity
  • paresis and general proprioceptive ataxia: (+/- vestibular ataxia)+
  • reduced or absent postural reactions+
  • deficits in CNIII-CNXII
  • increased muscle tone and cervical hyperesthesia possible
  • CVRS abnormalities possible

+ in all limbs or IPSILATERAL to lesion

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6
Q

What is decerebrate rigidity?

A

decerebrate rigidity is characterized by opisthotonus and extension of all limbs

  • usually the animal is stuporous or comatose (c.f. Decerebellate they are often awake and alert)
  • this is due to loss of descending input to the brain stem structure responsible for flexion and extension of the limbs
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7
Q

What are the clincial signs of a midbrain lesion?

A

dysfunction of the red nucleus, CNIII, and CNIV

(1) red nucleus
- motor function and gait generation (note: rostral lesions will cause contralateral and caudal lesions will cause ipsilateral reaction deficits)

(2) CNIII (oculomotor)
- controls medial rectus, dorsal rectus, ventral rectus, and ventral oblique extraocular muscles
- parasympathetic constricts pupil by relaxing the iris
- motor dysfunction = lateral strabismus and ptosis
- parasym. dysfunction = mydriasis +/- anisocoria

(3) CNIV (trochlear)
- controls CONTRALATERAL dorsal oblique extraocular muscle (only CN contralateral to brainstem nucleus)
- motor dysfunction: lateral rotation of pupil (contra. if troclear nucleus, ipsi. if troclear nerve axon)

easy to see in cats with slit eyes

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8
Q

What are the clincial signs of a pons lesion?

A

dysfunction of the pontine reticular formation and CNV

(1) pontine reticular formation
- motor function and gait generation, always ipsilateral

(2) CNV (trigeminal)
- facial sensation (opthalimic, maxillary, mandibular), and motor to muscles of mastication
- sensory dysfunction: reduced facial sensation (absent palpebral/corneal reflex, neurotrophic keratitis due to reduced tearing/blinking)
- motor dysfynction: atrophy of jaw muscles + potential enopthalmos if pterygoid affected (if bilateral -> dropped jaw, but this can also be due to trigeminal neuropathy, botulism, etc)

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9
Q

What are the clincial signs of a medulla oblongatta lesion?

A

dysfunction of the medullary reticular formation and CNVI-XII

(1) medulalry reticular formation:
- motor function and gait generation, always ipsilateral

(2) CNVI (abducens)
- controls lateral rectus and retractor bulbi extraocular muscles
- motor dysfunction: medial strabismus and failure to retract eye

(3) CNVII (facial)
- senses concave aspect of pinna, rostral 2/3 tongue, controls muscles of facial expression, P/S for tear production/salivary glands/nasal glands
- sensory dysfunction not easily appreciated
- motor dysfunction: lack of blink (exposire keratitis), absent/reduced menace, facial asymmetry (in LA: horse nose deviates to unaffected side and ear droop in both horse and cow)
- P/S dysfunction: KCS, dry nose (xeromycteria)

(4) CNVIII (vestibulochochlear)
- key in hearing (cochlear) and balance (vestibular)
- sensor dysfunction: hearing loss and vestibular disease
- hearing loss can be conductive (acquired): physical obstruction - debris or mass - in ear; it can be sensorineural (congenital or acquired): sensory hair cell loss, prevalent in dalmations, white cats w/ blue eyes, etc

(5) CNIX and CNX (glossopharyngeal and vagus)
- dysfunction: dysphagia, dysphonia, laryngeal paralysis, megaesophagous, P/S salivary (IX) or abdominal/thoracic viscera (x) dysfunction, dysautonomia (mydriasis, GI signs)

(6) CNXII (hypoglossal)
- dysfunction/atrophy of tongue muscles and deviation to affected side

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