GLM MTB step3 Neurology Flashcards
How do strokes/TIA present
“1) sudden onset of one-sided body weakness.
2) one-sided facial weakness and aphasia
3) partial or total loss of vision (transient)
4) Stoke spares upper third of face (from eyes up)
“
What is the cause of stroke/TIA
“decreased or altered cerebral blood flow
“
How are strokes different from TIA
“-The difference is based on time
1) Strokes last >24 hrs w/ permanent neuro deficits
2) TIA symptoms last <24 hrs & resolve completely
“
Which part of the face is spared in stroke patients
upper third (from eyes up)
Name the different types of strokes
“1) 80% ischemic (from emboli or thrombosis)
2) 20% hemorrhagic
“
Which type of stroke presents with more sudden symptoms emboli or thrombosis
emboli
What is amaurosis fugax
“transient loss of vision in TIA
“
What type of vision loss is seen in TIA
transient loss (amaurosis fugax)
What is the cause of amaurosis fugax
“decrease blood of branch of the carotid artery (ophthalmic artery)-> decrease in retinal circulation -> causes retinal hypoxia
“
What is the origin of TIA
thrombosis or emboli
Can TIA be caused by hemorrhage? Why or why not?
No; because hemorrhages don’t resolve within 24 hrs
A 67-year-old man with a history of hypertension and diabetes comes to the emergency department with a sudden onset of weakness in the right arm and leg over the last hour. On exam, he cannot lift the bottom half of the right side of his face. What is the best initial step? a. Head CT with contrast b. Head CT without contrast c. Aspirin d. Thrombolytics e. MRI
Answer: The correct answer is B.
Prior to administering thrombolytics or any anticoagulation, you need to *rule out hemorrhagic stroke, which is a contraindication to thrombolytics.*
You cannot even give aspirin without doing a head CT first.
Thrombolytics are indicated within the first *3 hours* of the onset of the symptoms of a stroke.
Remember, 20% of strokes are hemorrhagic.
You do not need contrast to visualize blood, contrast is used to detect cancer or infection, such as an abscess.
What can be visualized with contrast
cancer and infections
Symptoms of anterior cerebral artery lesion
“1) lower extremity weakness (contralateral in the case of unilateral arterial occlusion)
2) upper extremity weakness (contralateral in the case of unilateral arterial occlusion)
3) Personality changes or psychiatric disturbance
4) Urinary incontinence
“
Symptoms of Middle cerebral artery lesion
“1) upper extremity weakness (contralateral in the case of unilateral arterial occlusion)
2) Aphasia
3) Apraxia/neglect
4) The eyes deviate towards the side of the lesion
5) Contralateral homonymous hemianopsia, with macular sparing
Difficulty with A-B-Cs in M-C-A””
A-Apraxia
B-Blindness in corresponding half of the visual field (contralateral homonymous hemianopsia)
C-Contralateral Clumsiness of arm, face. — Leg is somewhat spared.
M-Memorization difficulties
C-Calculation difficulties
A-Aphasia with language-dominant hemispheral involvement
“
What is apraxia/neglect
“apraxia-motor disorder caused by damage to the brain, in which someone has difficulty with the motor planning to produce speech
neglect-
“
What is aphasia
acquired language disorder caused by damage to the brain.This class of language disorder ranges from having difficulty remembering words to losing the ability to speak, read, or write, but does not affect intelligence
Symptoms of posterior cerebral artery lesion
1) Prosopagnosia (inability to recognize faces)
Posterior cerebral artery (PCA) occlusion: P-O-S-T
P-Proximal fling movements
O-Occipital lobe infarction results in contralateral homonymous hemianopsia which may be complete
S-Speech and Spelling maintained, but unable to read fluently
T-Thalamic syndrome
1) Contralateral loss of pain and temperature sensations.
2) Visual field defects (contralateral hemianopia with macular sparing).
3) Prosopagnosia (inability to recognize faces)
4) Superior Alternating Syndrome (Weber’s syndrome)
5) Ipsilateral deficits of oculomotor nerve,
6) Contralateral deficits of facial nerve (only lower face, upper face receives bilateral input), vagus nerve and hypoglossal nerve
7) Horner’s Syndrome:
- ipsilateral partial ptosis
- upside-down ptosis (slight elevation of the lower lid)
- anhidrosis
- miosis
Symptoms of Vertebrobasilar artery lesion
“1) Vertigo
2) Nausea and vomiting
3) May be described as a ““drop attack””
4) Vertical nystagmus
5) Dysarthria and dystonia
6) Sensory changes in face and scalp
7) Ataxia
8) Labile blood pressure
vertebral-basilar circulation: 4D
- Dizziness
- Diplopia
- Dysarthria
- Dysphagia
Vertebro BANDS
- Vertigo
- Nausea and vomiting
- May be described as a ““drop attack,”” LOC
- Vertical nystagmus
- Dysarthria and dystonia
- Sensory changes in face and scalp
- Ataxia
- Bilateral findings”
Symptoms of lacunar infarct lesion
“P-BASH
1) There must be an absence of cortical deficits.
2) Ataxia
3) Parkinsonian signs
4) Sensory deficits
5) Hemiparesis (most notable in the face)
6) Possible bulbar signs
Lacunar infarct: ““Lacunar”” from the Latin for G-A-P or- D-I-S-P-A-R-I-T-Y
G-deep Gray matter: basal ganglia
A-Atherosclerosis
P-hyPertension
D-Dysarthria and a contralateral clumsy hand or arm due to infarction in the base of the pons or in the genu
of the internal capsule. (20%)
I-Internal Capsule: Lacunae in the posterior limb of the Internal capsule may cause pure motor hemiplegia
involving the face, arm, leg, foot. (60%)
S-Subcortical, capsular, or thalamic lacunae
P-Pontine lesions
A-Ataxic hemiparesis due to an infarct in the base of the pons
R-Rare: Lacunae in the anterior limb of the Internal capsule may cause severe dysarthria with facial weakness.
I-Ipsilateral ataxia (arm/leg) with leg weakness: Pontine lesion (rare)
T-Thalamus: Lacunae in the Thalamus may cause pure sensory stroke (10%)
y-V-Ventrolateral Thalamic lacunae
BASH
Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)
- There must be an absence of cortical deficits.
- Ataxia
- Parkinsonian signs
- Sensory deficits
- Hemiparesis (most notable in the face)
- Possible bulbar signs
Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)”
What is Dysarthria and dystonia
“dysarthria-condition in which problems effectively occur with the muscles that help produce speech, often making it very difficult to pronounce words.
dystonia-sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements may resemble a tremor.
“
List Parkinsonian signs
“M-BIRTH
1) Tremor at rest
2) Bradykinesis
3) Postural instability
4) rigidity
5) mask-like facies=hypomimia
6) small hand writing=micro???
T - Tremor - Involuntary trembling of the limbs (resting tremor)
R - Rigidity - Stiffness of the muscles
A - Akinesia - Lack of movement or slowness in initiating and maintaining movement
P - Postural instability - Characteristic bending or flexion of the body, associated with difficulty in balance and disturbances in gait
“
What is a bulbar sign
“1) Bulbar relates to the *medulla*.
2) Bulbar palsy is the result of diseases affecting the *lower cranial nerves (VII-XII). *
3) A speech deficit occurs due to *paralysis or weakness of the muscles of articulation* which are supplied by these cranial nerves.
“
Symptoms of Posterior inferior cerebellar artery lesion
“VICH
1) ipsilateral face
2) contralateral body
3) Vertigo and Horner’s symptoms
Horner’s Syndrome (Oculosympathetic paresis) is a rare neurologic condition whose symptoms and signs include:
Ptosis (drooping eyelid)
Anhidrosis (inability to sweat).
Miosis (pupil constriction)
Horner’s syndrome can be caused by any set of sympathetic nerve fiber injuries. Horner’s syndrome is generally classified into Central and Peripheral.
Central: Sympathetic nerves start in the brain and then travel down to the spinal cord and into the chest.
Peripheral: Sympathetic nerves start from the chest to the neck, arteries, head, and into the eyes.
Another feature of Horner’s syndrome is loss of ciliospinal reflex (pupil dilates when pressure / pain applied to neck or face. Patients with Horner’s syndrome also experience Enophthalmos (posterior displacement of the eyeball). These features can all be remembered by the mnemonic ““SAMPLE””
S: Sympathetic Nerve Fiber Injury
A: Anhidrosis
M: Miosis
P: Ptosis
L: Loss of ciliospinal reflex
E: Enophthalmos
“