2.7 Principles of Brainstem Disease Flashcards
What does the brainstem consist of?
the midbrain, the pons, and the medulla
Summary: what is the most important information to know about the brainstem?
- 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
What is the function of the brainstem?
- 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
What structures arise in the midbrian, pons, MO (and RF)
- 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)
What are the clinical signs of brainstem disease?
- 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
What is decerebrate rigidity?
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
What are the clincial signs of a midbrain lesion?
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
What are the clincial signs of a pons lesion?
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)
What are the clincial signs of a medulla oblongatta lesion?
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