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Chika- SF2 > Neurological Disorders I- Oyawusi > Flashcards

Neurological Disorders I- Oyawusi Flashcards

1
Q

NEED TO KNOW

A
  • compare and contrast upper motor neurons and lower motor neuron lesions with particular reference to cranial nerve 7 (facial weakness)
  • cortical gray matter in the cerebral hemisphere is where the upper motor neurons are

Irritation of the cortical grey matter causes seizures

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2
Q

What is the difference between CNS and PNS?

A

CNS: brain and spinal cord

PNS: the periphery of the structures of the brain and spinal cord

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3
Q

What is the cortical grey matter in the cerebral hemisphere?

A

upper motor neurons

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4
Q

What is the deep White matter in the cerebral hemisphere?

A

subcortical

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5
Q

What is the deep gray matter in the cerebral hemisphere?

A

thalamus, basal ganglia, hypothalamus

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6
Q

What is the basal ganglia?

A
  • caudate nucleus
  • putamen
  • globus pallidus internus and externus
  • subthalamic nucleus
  • substantia nigra
  • red nucleus
  • peripheral nuclei (claustrum, amygdala)

all these have connections that affect nuclei that affect your motor

direct pathway—increased movement: tremors, chorea, hemiballismus

indirect pathway—decreases movement: Parkinson’s disease

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7
Q

What are the hallmarks of basal ganglia disorders?

A
  • involuntary movements
  • bradykinesia
  • rigidity
  • gait, posture, and equilibrium disturbances
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8
Q

What is the difference between resting tremor and essential tremor?

A

In PD, the tremor is mostly seen at rest, when the body part is not being used, and may be referred to as “resting tremor.”

In ET, the tremor occurs mostly during action or movement, such as when writing, eating, or holding a posture.

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9
Q

What is chorea?

A

dance like movement

is a long-term complication of streptococcal infection

-in Huntigton dz

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10
Q

What is chorea?

A

dance like movement

is a long-term complication of streptococcal infection

  • in Huntington dz
  • huntingtin protein gene is altered
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11
Q

What are the characteristics of upper motor neurons?

A
  • Diffuse Weakness whole arm, leg etc.
  • Spasticity
  • Hyper-reflexia
  • Babinski’s reflex
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12
Q

What are the characteristics of lower motor neurons?

A
  • Segmental Weakness
  • Flaccidity
  • Hypo or Areflexia
  • Atrophy
  • Fasciculations
  • Fibrillations (don’t see but hear with EMG)
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13
Q

KNOW THIS

Irritation of the cortical grey matter causes what?

A

seizures (positive finding!!)

tonic-clonic followed by an ictal phase (brain is like ah can relax)

absence (seizure that affects children 5-13 yrs, 70% will age out of it)

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14
Q

What is the difference between simple focal, partial complex, and generalized seizures?

A

Focal seizures (previously called partial seizures) start in one part of the brain and affect the part of the body controlled by that part of the brain.

Primary generalized seizures involve the whole brain and therefore involve the whole body. There are many types of generalized seizures – some convulsive, others nonconvulsive.

Complex partial seizures, also called focal onset impaired awareness seizures, are the most common type for adults who have epilepsy

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15
Q

Destruction of cortical gray matter include what?

A

acite: altered sensorium; altered mental status

Chronic:

  • dementia
  • Minimally conscious state
  • alzheimer disease
  • persistent vegetative state
  • frontotemporal dementia

stroke, neurodegenerative disorders PD with amyloid plaque

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16
Q

Right parietal lobe syndrome

A
  • hemispatial neglect

- agraphesthesia

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17
Q

What are symptoms of Gerstmann syndrome?

A
  • hemispatial neglect
  • Acalculia
  • finger agnosia
  • agraphia
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18
Q

Frontal lobe

A

Expressive aphasia (Broca´s aphasia)

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19
Q

Temporal lobe

A 
Temporal Lobe
Sensory aphasia (Wernicke´s aphasia)

Complex Partial Seizures: are typically associated with auras

Transient global amnesia: destruction of both hemisphere

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20
Q

Aura is the warning sign that this type of seizure is getting ready to occur.

A

Complex Partial Seizures temporal lobe seizures

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21
Q

Occipital Lobe

A
  • Contralateral Homonymous Hemianopsia (sparing of the macula—foveal sparing)
  • Visual agnosia: can’t look at a car and say its a car
  • Prosopagnosia
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22
Q

If there is irritation of frontal eye field what occurs?

A

Contralateral Gaze Deviation

-affecting PPRP

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23
Q

If there is destruction of frontal eye field what occurs?

A

Ipsilateral Horizontal Gaze

24
Q

Parietal lobe is the major what area? What occurs with lesions there?

A

sensory area !!

dominant (left hemisphere) lesion will result in Gerstmann syndrome

in the right hemisphere will result in hemineglect

25
Q

A 56-year-old woman with an extensive history of alcohol consumption and a 25 pack-year smoking history presented to a local emergency department with her son because of persistent worsening of her mental status. Her son noticed that she was progressively less attentive and had depressed psychomotor speed.

Examination revealed she was mildly disoriented, with decreased attention speed, mild dysarthria, and bilateral symmetric upper extremity tremor. She had a wide-based gait with no ability to do tandem gait.

What is she suffering from?

A
  • extensive history of alcohol consumption
  • AMS (metabolic disorder)
  • wide-based gait (gait disturbance probably with balance; vermis of cerebellum is being affected)
  • bilateral symmetric upper extremity tremor (had a global presentation)

SO patient has a metabolic disorder!

decreased albumin (2.8) secondary to chronic alcohol use

A diagnosis of hepatic failure was made, and she was treated for minimal hepatic encephalopathy with lactulose and rifaximin, which resulted in significant improvement of her neuropsychiatric status.

26
Q

72 y/o man with HTN, with no prior CVA, but severe CAD s/p two prior stents was well when he went to bathroom at 3 am. At 6 am, his wife heard him fall and found him slumped on the side of the bed.

He was unable to move his right side and was mute. She called 911 and he was brought to the ER.

A

HTN

CAD risk factor for cerebrovascular disease

right sided weakness and mute affects left side of brain (right hemispheric stroke)

dense left gaze (Frontal eye fields are affected) and right facial droop

look for intracranial pressure to differentiate between ischemic and hemorrhaging stroke: blown pupil, papilledema

no headache
bleed was characterized as hyperintensity

mostly ischemic stroke we know 80% are; saw a hyperdense MCA sign on the CT

27
Q

What is an area that could have a small lesion but have overall very huge impact?

A

internal capsule: is compact with sensory and motor fibers

otherwise you’re expecting a very large stroke to cover the cortex

  • motor deficits
  • sensory deficits
  • visual deficits

Remember

28
Q

If there is an absence of cortical deficits then its most like

A

deep like altered sensorium

29
Q

What is the basal ganglia?

A

a grouping of deep gray matter that has influence on motor

has communication with thalamus that goes to premotor cortex

can cause an increase or decrease in movement

30
Q

How is essential tremor being treated?

A

Deep brain stimulation of the VIM thalamic nucleus modifies several features of essential tremor

31
Q

What is the hallmark of Huntington dz? Parkinson’s disease?

A

chorea

resting tremors, cogwheel rigidity, bradykinesia, unsteady/shuffling gait

32
Q

A 65-year-old HIV-positive man began having involuntary flinging movements of the right arm and leg, which became progressively worse over the course of 1 month, making gait and use of the right hand difficult. On exam, he had continuous wild, uncontrollable flapping and circular movements of the right arm and occasional jerky movements of the right leg, with an unsteady gait, falling to the right. The remainder of the exam was unremarkable.

A

there is hemiballismus (subthalamic nuclei on the left may be involved)
a lesion on left side of brain

flapping and circular movements of the right arm right leg: sound like choreoathetoid movement; localize the striatum

unsteady gait: maybe cerebellum is involved

it is not sudden so it is progressive (maybe a lesion growing)

Given the patient’s age, a lacunar infarction in the left subthalamic nucleus or left striatum is the most likely diagnosis. A small hemorrhage in these locations is also possible. Nevertheless, the history of gradual onset over the course of a month would be somewhat unusual for either an infarct or a hemorrhage. Especially because the patient has a history of HIV, other brain lesions should also be considered. The most common intracranial mass lesions in patients with HIV are toxoplasmosis and primary central nervous system lymphoma, either of which could occur in the subthalamic nucleus or striatum

33
Q

A 53-year-old right-handed man was referred for a second opinion regarding progressive bradykinesia, tremor, rigidity, and unsteady gait.

The patient was well until 10 years previous, when, while working as a fireman, he had noticed some slowness and difficulty using his right arm. This symptom gradually progressed, and 2 years later he had to change jobs and began working for the phone company. In the interim he developed occasional shaking of the right arm and right leg.

A

Parkinsonians

Parkinson’s disease is caused by loss of dopaminergic neurons in the substantia nigra pars compacta.

Dopaminergic neurons in the substantia nigra normally project to the striatum.

Loss of dopaminergic excitation of the direct pathway and loss of dopaminergic inhibition of the indirect pathway both ultimately result in more inhibitory output from the internal segment of the globus pallidus (and the substantia nigra pars reticulata) to the thalamus. This, in turn, leads to less excitatory activity from the thalamus to the motor and premotor cortices, resulting in a hypokinetic movement disorder

34
Q

The thalamus is the relay organ for what information?

A

for sensory, motor, and limbic information,
all senses EXCEPT for smelling

VPL and VPM:All sensations from body ad face respectively

LG and MG – Visual & Auditory

VL and VA - Basal ganglia & VL for Cerebellum; VL plays a role in terms of relaying information from the cerebellum

Anterior – Limbic System (Amygdala, Hippocampus, Parahippocampus, Fornix, Mammillary bodies, Anterior Nucleus of Thalamus & Cingulate Gyrus)

35
Q

What are the functions of the hypothalamus?

A

Vegetative Functions – Internal Mileau regulation. Temperature, Appetite, Thirst

Endocrine – Anterior & Posterior Pituitary connections directly or through portal circulation. Hormonal levels should be tested

Limbic system – Mammillary bodies

Autonomic Nervous System – Sympathetic Nervous System

Optic Chiasm Function must be tested (if there are lesions like gliomas in the hypothalamus that could affect the function of the optic chiasm)

36
Q

What is the functional of the cerebellum?

A

is connected to brainstem through peduncles

Superior (efferent) Midbrain to CONTRALATERAL red nucleus to VL nucleus of thalamus to pre-motor cortex (decussates)

Middle –fronto-ponto-cerebellar to CONTRALATERAL Pons

Inferior (afferent) Medulla

Vermis is for balance, posture, and equilibrium and ataxia

Hemispheres is for ipsilateral dysmetria (finger to nose), intentional tremors, dysdiadochokinesis (incoordination of rapid movements), rebound, and hypotonia

37
Q

What is the hallmark of brainstem lesions?

A

crossed clinical manifestations

All cranial nerves are ipsilateral and exit from (or enter) the ventral part of the brain stem –EXCEPTION – Cranial Nerve 4 or Trochlear –supplies the superior oblique muscle.

Cortico-spinal tract always causes contralateral deficit in brain stem lesions

Lesion is always at the level of origin of the manifesting cranial nerve and on the same side as the cranial nerve manifestation

38
Q

What is the hallmark of cortical or capsular lesions?

A

the symptoms are all on the same side

39
Q

Tegmentum: give them tactile stimulus and they have extension posture. What is this called?

A

decerebrate rigidity: extension of upper and lower limbs

decorticate rigidity: flexion of the upper limb but extension of the lower limb

40
Q

What is the inferior medial pontine syndrome (foville syndrome)?

A

weakness of the face ipsilateral and contralateral weakness in the body

due to facial nucleus and corticospinal tract

41
Q

MLF syndrome

A

internuclear ophthalmoplegia

42
Q

How do you test for brainstem reflex at the level of the pons?

A

caloric test

43
Q

What is locked-in syndrome?

A

the only movement they can produce is with their eyes

due to the lesion of the terminal of the basilar artery
the corticobulbar, corticospinal, and CN III BILATERALLY

44
Q

What occurs in MS?

A

MLF connect oculomotor with abducens nucleus for horizontal gaze

destruction of the PPRP results in ipsilateral gaze palsy

45
Q

If a patient has an active seizure in the left frontal eye field where would the eyes move?

A

causes eye to look to the right

Left FEF–> Right PPRP which is controlling your eyes moving to the right

seizure is not a destructive lesion, it is hyperactivity
stroke is destructive

46
Q

If a patient has an stroke in the left frontal eye field where would the eyes move?

A

cause eyes to look to the left

47
Q

The PRPP is involved in ipsilateral gaze. How is MLF involved?

A

MLF is the fasciculus or connection that bridges to the PPRP from the frontal eye field

48
Q

What arteries perfuse the lateral medulla?

A

vertebral artery

PICA branches

49
Q

What are the signs of the lateral medullary syndrome/Wallenburg/Crossed Sensory syndrome?

A

Cranial Nerves 8, 9, 10, sensory 5

  • facial numbness
  • vestibular nuclei: nystagmus, vertigo, ataxia
  • nucleus ambiguus: info from CN IX and X so dysphagia and dysarthria
  • Horner’s syndrome: sympathetics so ptosis, sweating
  • loss of pain and temp on contralateral side of body
50
Q

What are signs of medial medullary syndrome?

A

Cranial Nerve 12
Crossed Corticospinal tract with hemiparesis
Various dorsal column manifestations

51
Q

Chief Complaint
A 22-year-old woman suddenly developed left posterior neck pain, vertigo, ataxia, left facial numbness, and hoarseness after chiropractic neck manipulation.
History
The patient had been well until 4 months previously, when she injured her neck in a car accident. She saw a chiropractor daily for neck pain. On the day of admission, after her neck was “snapped,” she suddenly felt increased pain in the left posterior neck region. As she left the chiropractor’s office, she felt dizzy and nauseated and staggered out to her car, falling toward the left. She noticed her vision bouncing or swaying (oscillopsia) but had no diplopia. She vomited twice, and when she reached home her husband noticed that her voice sounded hoarse. She also felt a numbness and tingling on the left side of her face. The symptoms did not improve after a brief nap, so she came to the emergency room.

A

It is all of a sudden
neck manipulation is a very common cause for dissection of the internal carotid artery

vestibular nuclei: vertigo, ataxia
sensory 5: left facial numbness
pain in the left posterior neck region

Pain in the left posterior neck region
Unsteady gait, falling toward the left
Left ataxia and dysrhythmia
Dizziness and nausea with right-beating nystagmus
Decreased pinprick and temperature sensation in the left face
Decreased left corneal reflex
Decreased pinprick and temperature sensation in the right limbs and trunk below the neck
Left ptosis, with small, reactive left pupil
Hoarseness, with decreased palate elevation on the left and decreased left gag reflex

The most likely clinical localization and diagnosis is, therefore, left lateral medullary syndrome, with left lateral medullary infarct caused by left vertebral dissection.

52
Q

What is the differences in signs for lesions in the cauda equina and those in the conus medullaris?

A

cauda equina: hyperreflexia
conus medullaris: areflexia

Guillain-Barre: lumbar tap for increased proteins in CSF

53
Q

A 56-year-old male auto mechanic had 1 month of episodic diplopia and unsteadiness and then suddenly developed persistent right face numbness, hearing loss, and right-sided clumsiness.
History
Past history was notable for severely elevated cholesterol and cigarette smoking. About 1 month prior to admission, the patient developed transient episodes consisting of light-headedness, nausea, unsteadiness “staggering like I was drunk,” diagonal diplopia with the right image higher than the left, perioral numbness, and a generalized headache. The episodes were precipitated by his standing up and walking around, lasted 5 or 6 minutes, and occurred up to four or five times per day. The episodes gradually improved over time and nearly stopped

A

Discussion  
The symptoms are strongly suggestive of brainstem dysfunction, possibly localized to the pons.
Given the patient’s vascular risk factors and the fact that the episodes occur in situations that may lower the patient’s systemic blood pressure (standing up), the most likely diagnosis is TIAs in the vertebrobasilar system, possibly caused by basilar stenosis. This is a potentially life-threatening situation, and the patient should be brought immediately to the hospital for evaluation including MRA, and for appropriate treatment.

54
Q

What are some hallmarks of spinal cord lesions?

A

Loss of pain and temperature up to a segmental level

Bowel & Bladder manifestations

Bilateral tract manifestations

Dissociated sensory loss

55
Q

What is the difference between Duchenne’s muscular dystrophy and Becker’s syndrome?

A

Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle degeneration and weakness. It is one of nine types of muscular dystrophy. DMD is caused by an absence of dystrophin, a protein that helps keep muscle cells intact. Increasing weakness of the respiratory muscles also makes them susceptible to pneumonia and other illnesses, and most die by the age of 20.

Becker muscular dystrophy is an X-linked recessive inherited disorder characterized by slowly progressing muscle weakness of the legs and pelvis. It is a type of dystrophinopathy. This is caused by mutations in the dystrophin gene, which encodes the protein dystrophin. Weakness is less severe and first appears a little later, at about age 12. They are usually able to walk until at least age 15, and many remain able to walk into adulthood. The pattern of weakness resembles that of Duchenne muscular dystrophy. However, very few adolescents need to use a wheelchair. Most people survive into their 30s or 40s.

56
Q

Polymyositis and Dermatomyositis

A

associated with rheumatological condition
changes in vasculature
CPK elevation

Chika- SF2 (63 decks)

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