Brainstem Flashcards

1
Q

cerebral aquaduct

A

common site of obstruction that results in noncommunicating hydrocephalus

periaqueductal gray contains neurons with opiod receptors that are stimulated by the spinomesencephalic component of the anterolateral system; these neurons function in the suppression of pain.

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2
Q

Lesion of corticospinal tract axons

A

in the brainstem above the decussation may result in spastic hemiparesis in the limbs contralateral and below the lesion

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3
Q

Complete lesion of the medial lemniscus

A

in the brainstem may result in a loss of touch, vibration, and pressure sensations in the upper and lower limb, neck, and trunk contralateral and below the lesion

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4
Q

Lesion of the spinothalamic tract

A

in the brainstem may result in a loss of pain and temperature sensations from the upper and lower limb, neck, and trunk contralateral and below the lesion

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5
Q

Horner’s Syndrome

A

patients with a lesion of the descending hypothalamic axons in the brainstem may have a central Horner’s Syndrome that is always ipsilateral to the side of the lesion. Patients with Horners have mitosis, ptosis, and andhydrosis.

They may also present with loss of pain and temperature sensations in the limbs and trunk contralateral to the lesion due to the proximity of the spinothalamic tract to the descending hypothalamic axons.

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6
Q

Lesion of MLF

A

Lesions of the MLF may result in internuclear opthalmoplegia which disrupts horizontal conjugate gaze and the vestibuloocular reflex

*MLF particularly susceptible to CNS disease such as MS and neurosyphilis

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7
Q

Oculomotor nerve lesions

A

All of the muscles that adduct the eyeball are innervated by CN III so a lesion may result in a laterally deviated eyeball (external strabismus) because of an inability to aDDuct eyeball

patients may have ptosis and parasympathetic deficits

preganglionic parasympathetic axons course in the peripheral part of CN III and are subject to external compression before the skeletal motor fibers. Initial signs of compression are therefore a dilated pupil, loss of the light reflex, and loss of the near response on the side of the lesion

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8
Q

Hypoglossal Nerve lesion

A

results in an ipsilateral paralysis of one half of the tongue and a deviation of the tip of the tongue on protrusion toward the side of the lesion

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9
Q

Glossopharyngeal nerve lesions

A

reduction in parotid secretions, difficult to use as diagnostic tool

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10
Q

Trigeminal nerve lesions

A

unilateral lesion of the motor fibers of CN V may result in a deviation of the jaw on protrusion toward the side of the lesion

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11
Q

Bell’s Palsy

A

lesions of the skeletal motor axons in the facial nerve may result in a complete paralysis of muscles of facial expression ipsilateral to the side of the lesion and hyperacusis due to weakness of stapedius

patients have weakness in the ability to wrinkle the forehead, shut the eye, flare a nostril, and show their teeth on the side of the lesion

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12
Q

Vagus nerve lesion

A

a lesion of the motor axons of vagus that arise from the nucleus ambiguus may result in an ipsilateral weakness of the soft palate and a nasal regurgitation of liquids. The tip of the uvula may deviate away from the lesion

a weakness of the pharyngeal muscles may result in difficulty in swallowing (dysphagia) and a weakness laryngeal muscles may result in hoarseness.

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13
Q

Lesions of the medulla

A

may affect fibers of CNs IX, X, or XII but not CN XI because the fibers of this arise from the cervical spinal cord

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14
Q

Accessory nerve lesions

A

occurs commonly outside the skull and results in a weakness in the ability to laterally rotate the scapula during abduction and a weakness in the ability to elevate the scapula. Accessory nerve lesions may also result in a weakness in the ability to turn the chin to the side opposite the lesion

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15
Q

Lesions of corticobulbar axons to the hypoglossal nucleus

A

the tongue muscles will not undergo fasiculations and atrophy and may deviate AWAY from the injured corticobulbar fibers (versus lesion of the hypoglossal nerve towards the injured side)

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16
Q

in a lesion of the corticobulbar axons to the nucleus ambiguus

A

the uvula may deviate toward the lesions fibers (versus the vagus nerve lesion where it deviates away)

17
Q

Patients with facial weakness - how to distinguish

A

differentiate between a lesion of CN VII and a lesion of the corticobulbar fibers to the facial motor nucleus

Patients with a facial nerve lesion: may have a complete paralysis of muscles of facial expression ipsilateral to the side of the lesioned nerve and have an inability to wrinkle the forehead, shut the eye, and flare a nostril, and a drooping of the corner of the mouth

Unilateral corticobulbar lesion may result in only a lower face weakness as evidenced by a drooping of the corner of the mouth on the side of the face contralateral to the lesioned corticobulbar fibers. These patients will be able to wrinkle their forehead and shut their eyes and will have an intact blink reflex.

18
Q

bilateral lesion of the solitary nuclei

A

may cause respiratory failure (respiratory failure may by preceded by ataxic respiration)

19
Q

Gag reflex

A

uses visceral sensory fibers in CN IX and skeletal motor fibers in CN X

20
Q

Cough reflex

A

uses both sensory and motor fibers in CN X

21
Q

Tirgeminal Neuralgia (Tic Douloureux)

A

trigeminal neuralgia is characterized by episodes of sharp, stabbing pain radiating over the territory supplied by mucosal or cutaneous branches of the maxillary or mandibular divisions of the trigeminal nerve

pain is frequently triggered by moving the mandible, smiling, or yawning or by cutaneous or mucosal stimulation

22
Q

Conductive hearing losses

A

result from interference of sound transmission through the external ear or middle ear. Middle ear infections children and otosclerosis in adults are common causes of a conductive hearing loss.

In conductive hearing loss, bone conduction is better than air conduction as a result of loss of the amplification provided by the middle ear.

Patients with conductive hearing loss will hear the vibrations better on the side of the defective external or middle ear because vibrations that reach the normal ear by both bone and air conduction interfere with each other, making the normal ear less sensitive.

23
Q

Sensorineural hearing losses

A

result from a loss of hair cells in the cochlea or from a lesion to the cochlear part of CN VIII or to any CNS auditory structure

24
Q

4 common causes of a sensorineural hearing loss at the cochlear level:

A

trauma from high intensity sound

infections

drugs

prebycusis: most common cause of sensorineural hearing loss in the elderly and results from progressive high frequency hair cell loss near the base of the cochlea.

25
Q

Ipsilateral sensorineural hearing loss

A

the lesion is most likely in the inner ear, CN VIII, or cochlear nuclei but not at higher levels of the central auditory system which contain neural structures that receive inputs from both ears.

26
Q

Lesion to CNS auditory structures in the brainstem:

A

above the cochlear nuclei, in the thalamus, or in the cortex may result in a slight bilateral hearing loss and a decreased ability to localize a sound source.

27
Q

Vestibular lesion

A

patients may have vertigo, an abnormal perception of rotation which may involve either the subject or the external space. The vertigo is usually severe in peripheral vestibular lesions and mild in central CNS lesions.

28
Q

Meniere’s disease

A

patients may have abrupt, recurrent attacks of vertigo lasting minutes to hours. The vertigo may be accompanied by tinnitus and an ipsilateral sensorineural hearing loss. Nausea, vomiting, and a sensation of fullness or pressure in the ear also are common during the acute episode.

The disease usually occurs in middle age and results from distention of the endolymph-filled spaces in the cochlear and vestibular parts of the labyrinth

29
Q

Nystagmus

A

slow, rhythmic oscillation of the eyes to one side followed by a fast reflex movement of the eyes in the opposite direction

it is usually horizontal, although rotatory or vertical nystagmus may also occur.

it is defined by the direction of the fast, or corrective phase.

It may result from a lesion of the labyrinth, vestibular nerve, or nuclei. It may also result from a metabolic disease or a lesion of the cerebellum, visual system (usually reflex centers and their connections), or cerebral cortex.

30
Q

Pathologic Nystagmus involving the vestibular nerve

A

an initial slow deviation of the eyes toward the side of the lesion in response to the pathology. A fast or corrective phase occurs in the opposite direction that is generated by the cerebral cortex.

In patients with a vestibular-evoked nystagmus the fast or corrective phase is away from the side of the lesion. A peripheral nystagmus is usually accompanied by vertigo. In a central lesion of the vestibular nuclei or cerebellum, the nystagmus may be bidirectional and may occur without vertigo.

31
Q

Caloric testing

A

evaluates the vestibulo-ocular reflex by introducing warm or cool water into an external auditory meatus

the direction of the fast phase of vestibular evoked nystagmus in a caloric test toward the warm water side and away from the cool water side is summarized by the COW (cool - opposite - warm - same)

32
Q

Caloric testing and the comatose patient

A

in a comatose patient with a nonfunctioning cerebral cortex but an intact brainstem caloric testing will only generate a slow deviation of both eyes, but not a fast or corrective phase.

In a comatose patient with a bilateral MLF lesion above the abducens nucleus, caloric testing will only result in a slow deviation of the abducting eye because adduction requires that the MLF be intact.

in a patient with a bilateral lesion to the vestibular nuclei, there will be no eye movement at all in response to caloric testing.

33
Q

brainstem lesions deficits

A

commonly result in signs or symptoms that begin with letter “d”

diplopia

a deviated eye, tongue, uvula, or mandible

dysphagia

dysphonia

a drooping eyelid

droopy face

34
Q

thalamic pain syndrome

A

commonly results from a lacunar stroke involving thalamoperforating branches of a posterior cerebral artery, which supply the ventrobasal complex

patients may have an impairment of all forms of somatic sensations in the body and limbs contralateral to the affected thalamus

central pain may also occur if the lesion affects the anterolateral system part of the ventrobasal complex. Patients have an initial analgesia which is replaced over time by spontaneous aching, burning pain, which is often excruciating, and a heightened sensation of pain is felt even after light cutaneous stimulation of the contralateral limbs or body. There is frequently a heightened sensation of cold or heat.

Pain in thalamic pain syndrome will not respond to anti-inflammatoryy analgesics which act to suppress pain at brainstem or spinal cord levels4

35
Q

lesions of the supraoptic and paraventricular nuclei

A

may result in diabetes insipidus which is characterized by polydipsia (excess water consumption) and polyuria

-may also be due to trauma to the hypothalamohypophysial tract