Brainstem Flashcards
cerebral aquaduct
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.
Lesion of corticospinal tract axons
in the brainstem above the decussation may result in spastic hemiparesis in the limbs contralateral and below the lesion
Complete lesion of the medial lemniscus
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
Lesion of the spinothalamic tract
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
Horner’s Syndrome
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.
Lesion of MLF
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
Oculomotor nerve lesions
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
Hypoglossal Nerve lesion
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
Glossopharyngeal nerve lesions
reduction in parotid secretions, difficult to use as diagnostic tool
Trigeminal nerve lesions
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
Bell’s Palsy
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
Vagus nerve lesion
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.
Lesions of the medulla
may affect fibers of CNs IX, X, or XII but not CN XI because the fibers of this arise from the cervical spinal cord
Accessory nerve lesions
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
Lesions of corticobulbar axons to the hypoglossal nucleus
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)
in a lesion of the corticobulbar axons to the nucleus ambiguus
the uvula may deviate toward the lesions fibers (versus the vagus nerve lesion where it deviates away)
Patients with facial weakness - how to distinguish
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.
bilateral lesion of the solitary nuclei
may cause respiratory failure (respiratory failure may by preceded by ataxic respiration)
Gag reflex
uses visceral sensory fibers in CN IX and skeletal motor fibers in CN X
Cough reflex
uses both sensory and motor fibers in CN X
Tirgeminal Neuralgia (Tic Douloureux)
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
Conductive hearing losses
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.
Sensorineural hearing losses
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
4 common causes of a sensorineural hearing loss at the cochlear level:
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.