68yoM diabetic patient felt unsteady and felt when power failure caused lights to go out in his living room, making the room very dark. Once power and lights returned he had no trouble standing and walking. Did sudden darkness cause his fall? How? Could this be related to his diabetes?
- Vision needed for postural stability. (Cerebellar and vestibular problems would have shown before the lights went out so we know it is a somatosensory problem.) Diabetic retinopathy and other neuropathies: diabetes affects vision, which affects proprioception.
22yoM brought to the ED via ambulance following a motorcycle accident. Patient cannot voluntarily move his arms or legs. He has no feeling below the neck and has lost all reflexes in arms, legs and trunk. Corneal reflexes were retained. Patient shows neither voluntary nor reflex movement below the neck. Where is the lesion in the spinal cord? Upper or motor neuron lesion?
- Patient is in spinal shock and has flaccid paralysis. Upper extremity paralysis indicates lesion is in cervical spine. Lower motor lesion is associated with flaccid paralysis; upper motor lesion would be associated with spastic paralysis and hyperreflexia.
What is spinal shock? Associated with flaccid or spastic paralysis?
- Spinal shock is a result of a spinal cord injury, most often complete transection. Initially presents as flaccid paralysis with absent reflexes caudal to the injury. Reflexes above remain intact.
Explain why one year after his accident this 22yoM pt would have strong withdrawal reflexes to noxious stimuli even though he does not “feel” any pain in response to stimuli. Stretch reflexes are abnormally brisk.
- Reflexes return post spinal shock as hyperreflexia, brisk stretch reflexes and strong nociceptive withdrawal reflexes. Motor and sensory are permanently lost.
At what age is an up going toe with Babinski reflex considered abnormal?
- At 3yo
What is the difference between voluntary and reflex movement?
- Voluntary requires higher brain area vs. reflex movement which occurs in spinal cord without connection to the brain.
64yo right-handed female present c/o HA, onset 2-3 weeks since landlord turned down the heat. No abnormalities on head and neck, cranial nerve or sensory examinations. Motor in the left hand seemed weaker and less coordinated than the right. Deep tendon reflexes were all brisker on the left than the right side. Extensor plantar reflex present on the left. Where does this indicate the lesion is? Do you think this is a localized infarct or a large hematoma?
- Babinski sign indicates UMN lesion could be anywhere from motor cortex along corticospinal tract. Lesion must be above thoracic spine since hand is affected. Hand and foot symptom occurred because pt had a large hematoma instead of localized infarct. CT scan revealed right frontal hematoma. Most people have language area in left hemisphere.
50yoM presents c/o dizziness when he rolls over in bed or turns his head a certain way. He never feels dizzy when he is merely standing, sitting or lying down in one position. Simple position testing for vertigo and nystagmus is done. What is probably causing this patient’s symptoms? Is it curable?
- Problem is most likely semicircular canals because pt experiences dizziness when rolling over. Utricle and saccule function in a linear acceleration and thus pt would feel dizzy when in one position, not just with movement. Turning head causes sx because a piece of otolith membrane breaks off and enters the posterior semicircular canal (which senses head turns). Otolith membrane fragment causes gravity to give signal of turning. Yes it is curable.
79yoM presents to ED via ambulance. Pt initially displayed decorticate posturing in response to noxious peripheral stimuli. 30 minutes later he displayed decerebrate posturing. Shortly after he developed Cheyne-Stokes respiration. The patient had previously filed a DNR request at his nursing home so no resuscitation efforts were made when his heart stopped beating soon afterward. What is decorticate posturing? Decerebrate? What could have caused this pt to switch from decorticate to decerebrate posturing? What could have caused the Cheyne-Stoke respirations?
- Decorticate is upper midbrain or above (arms flexed, legs extended) whereas decerebrate is upper pons (both arms and legs extended). Large hemorrhage continuing to push down would cause pt to go from a decorticate (upper midbrain lesion) to decerebrate (upper pons). A supratentorial lesion has extended through the tentorial notch to the upper pons. This means the pt is deteriorating. As the bleeding pressure spreads lower, the brainstem where breathing is controlled is affected, causing him to lose his breathing and start Cheyne-Stokes.
64yoM c/o R handed weakness following a cardiac arrest. Pt had a hx of HTN and cigarette use. He collapsed in church, was given bystander CPR and then successful electrical defibrillation by EMTs. Pt was admitted to cardiac ICU and found to have episodes of rapid A-fib. Several days after admission, pt was noted to have weakness of the R hand and a neurology consult was requested. What disease process most likely caused his heart attack and weakness?
- A-fib promotes clot formation. (Blood pooling in atrium; static blood => clots => embolize) Clots leave the aorta and go into coronary circulation first, causing the MI. Clots could also go to brain and cause a stroke involving the motor cortex.
Pts mental status was alert and oriented with no language or memory problems. Cranial nerves were normal, including no facial weakness. Sensory WNL. Motor 5/5 except right hand and wrist. R wrist flexion/extension/grip 3/5, R finger extension/abd-/adduction/thumb opposition 0/5. What is the dx? What artery is likely involved?
- Small ischemic stroke (need more tests to ID motor cortex or red nucleus). Small area of motor cortex or internal capsule involved (but less likely IC or more things would also likely be damaged due to the structures being so close together). Middle cerebral artery. Since right had is involved, left middle cerebral artery.
70yoM presents to the ED c/o N/V and unsteadiness. Pt is a semi-retired janitor, pmhx HTN. Symptoms onset suddenly while at work. On neuro exam, pt had mildly slurred speech with slowed tongue movements, dysmetria on finger-to-nose testing on left as well as dysmetria on heel-to-shin on left and left dysdiadochokinesia. Upon standing, pt fell to left even with eyes open. On the basis of patient’s signs and symptoms, what is the lesion? What is the most likely dx? What are some other possibilities? Do you expect pt to improve?
- Cerebellar lesion, likely secondary to hypertension. MRI showed left superior cerebellar artery infarct involving the left superior peduncle and left superior hemisphere. No obvious embolic source was found. Ataxia gradually improved and one week later, patient had normal speech with minimal left ataxia. Small enough area of brain that plasticity will make up for injury and pt can recover. (Remember there was problems with articulating, not language, thus being a cerebellar problem.)
67yoM presents with complaint of disturbed sleep. His wife said that several times a week her husband awoke her very late at night by his loud talk and even shouting. He was apparently still asleep and very difficult to awaken. When finally awakened he would remember violent dreams. Sometimes he would flail around in his sleep fall out of bed. Wife no longer feels safe sharing a bed because she is often hit by his wild arm movements. Last time this happened he started choking her and reported a dream where he was fighting off a robber. What would a sleep study show? What is the most likely diagnosis? Can the condition be cured or at least treated?
- Sleep study would show REM associated sleep disorder – patient is not paralyzed (atonia) during REM as he should be. Treatment is pharmacological – don’t worry about it until next fall. :)
69yo R-handed woman brought to ED by husband due to sudden onset L-sided weakness. Moderate left hemiparesis, partial left sided sensory deficits, left visual deficit (homonymous hemianopia). Both before and after this exam she denied having any problem at all. What is going on?
- Lesion after optic chiasm (or pt would have bitemporal hemianopia). Homonymous hemianopia could be optic tract lesion or lateral geniculate nucleus or optic radiation. Since visual loss is contralateral and her symptoms are left, the defect is on the right. Pt has no problems before or after exam because she has contralateral neglect, indicating a parietal lesion of the nondominant hemisphere (right hemisphere for most people).
69yoF was asked to hold out both arms and she held up only the right one but insisted that both arms were out. Later she referred to her left arm as an artificial limb that the doctors had given her. She said the reason she couldn’t walk was due to knee problems. What probably caused this woman’s problems? Why did she seem unaware of her sensory and motor deficits? What kind of neurological lesion could cause these problems?
- Stroke involving non-dominant right hemisphere. Pt is ignoring left side of her body and makes up a reason to make sense of it.
48yoM presents with cc of increasing hearing loss in left ear and dizziness that causes problems with balance. Gradual onset of hearing loss in his left ear. Pt felt unsteady sometimes when walking especially after quick turn. He recently developed hissing noise in his left ear and balance problems getting worse. No pmhx, no current medications. PE WNL. Neuro exam: hearing loss on left with poor speech discrimination. Weber test: sound was louder in right ear. What do the Weber test results mean?
- If conductive hearing loss, sound lateralizes to bad ear. If sensorineural loss, sound lateralizes to good ear. Thus, pt has sensorineural hearing loss since sound localized to better ear (right ear).
Brainstem auditory evoked potential study was done. There was a prolongation in the interlatency difference between waves I and II on the left side. Audiogram showed sensorineural hearing loss in the left ear. What does the BAEP show? What could happen with the cochlear nerve that would result in both auditory and vestibular problems? What do you expect MRI to show?
- BAEP are small electrical voltage potentials in response to auditory stimuli. Graph shows voltage over time. Between 1 and 2 seconds is the cochlear nerve. If pt had a latency between 3 and 4, we’d think the problem was further along the auditory pathway. Both acoustic neuroma and vestibular schwannoma would result in auditory AND vestibular problems. MRI showed well-circumscribed enhancing lesion without surrounded edema extending from the internal auditory canal into the left cerebellopontine angle.
23yo R-handed woman presents to the ED with sudden onset visual disturbance. She reports the previous day she noticed some pain in her right eye, especially when looking around. This am she awoke and realized she was unable to see with her right eye. She has never experienced anything like this before. She is otherwise in good health, does not take any daily meds. PE showed complete vision loss in R eye with absent pupillary response. What do we call this? She denies pain at this time, EOM full, visual field intact L eye, neuro exam WNL otherwise.
- Marcus Gunn pupil.
What is a Marcus Gunn pupil caused by? How would the pupil respond to light shone in the affected eye? How would the pupil respond to having light shone in the normal eye?
- Marcus Gunn pupil is an afferent pupillary defect in the affected eye, associated with pupillary light reflex. Optic nerve issue prior to the chiasm, so light shone in the unaffected eye will result in consensual constriction but when light is shone in the affected eye, the Marcus Gunn pupil will no longer constrict (afferent defect – passively relaxes and dilates).
Which cranial nerve is the afferent limb and efferent limb of the pupillary light reflex? Explain the path of the reflex. What does the pupillary muscle do? Ciliary muscle? Parasympathetic or sympathetic innervation?
- CN II is the afferent limb; CN III is the efferent limb. Light is shone in the eye. CN II sends input to pretectum. Pretectum relays signal to the Edinger-Westphal nucleus (origin of the parasympathetic preganglionic fibers to ciliary ganglion), which results in pupil constriction. Pupillary muscle functions in pupil constriction. Ciliary muscle changes shape of lens for accommodation.
CSF studies were normal. MRI scan revealed increased signal and contrast enhancement in the R optic nerve. What is the dx? Treatment? Will she improve?
- Dx = optic neuritis. Often associated with MS. Treat with high dose steroids (methylprednisolone). Vision should improve in 8 weeks.
