Week 3

Question 1

trigeminal neuralgia

Answer 1

Process: Vascular compression of CN V, usually near entry to pons leading to focal demyelination, aberrant discharge. 10% with causative intracranial lesion

Location: Cheek, jaws, lips, or gums; trigeminal nerve divisions 2 and 3 > 1

Quality and Severity: Shocklike, stabbing, burning; severe

Onset: Abrupt, paroxysmal

Duration: Each jab lasts seconds but recurs at intervals of seconds or minutes

Course: May recur daily for weeks to months then resolve; can be chronic progressive.

Associated Sx: Exhaustion from recurrent pain

Agg Factors: Touching certain areas of the lower face or mouth; chewing, talking, brushing teeth

All Factors: Medication; neurovascular decompression

Question 2

Assessment of stroke requires careful history taking and a detailed physical examination, and should focus on three fundamental questions:

Answer 2

What brain area and related vascular territory explain the patient’s findings?
Is the stroke ischemic or hemorrhagic?
If ischemic, is the mechanism thrombosis or embolus?

Stroke is a medical emergency, and timing is of the essence.
-Answers to these questions are critical to patient outcomes and use of antithrombotic therapies.

Question 3

contralateral leg weakness (vascular territory, additional comments)

Answer 3

vascular territory: anterior circulation- anterior cerebral artery (ACA)

additional comments: The internal carotid arteries supply the anterior circulation, providing blood flow to the anterior and middle cerebral arteries

Question 4

Contralateral face, arm > leg weakness, sensory loss, visual field loss, apraxia, aphasia (left MCA), or neglect (right MCA) (vascular territory, additional comments)

Answer 4

vascular territory: Anterior circulation—middle cerebral artery (MCA)

additional comments: Largest vascular bed for stroke, so most common territory affected

Question 5

Contralateral motor or sensory deficit without cortical signs (such as aphasia or neglect) (vascular territory, additional comments)

Answer 5

vascular territory: Subcortical circulationa—lenticulostriate deep-penetrating branches of MCA

additional comments: Small vessel subcortical lacunar infarcts in internal capsule, thalamus, or brainstem. Five classical syndromes are seen: pure motor stroke (hemiplegia/hemiparesis), pure sensory stroke (hemianesthesia), ataxic hemiparesis, clumsy-hand/dysarthria syndrome, and mixed sensorimotor stroke

Question 6

Contralateral visual field loss (vascular territory, additional comments)

Answer 6

vascular territory: Posterior circulation—posterior cerebral artery (PCA)

additional comments: The paired vertebral arteries join to form the basilar artery, which supplies the posterior circulation. Bilateral PCA infarction causes cortical blindness but preserved pupillary light reaction.

Question 7

Dysphagia, dysarthria, tongue/palate deviation, and/or ataxia with crossed sensory/motor deficits ( = ipsilateral face with contralateral body) (vascular territory, additional comments)

Answer 7

vascular territory: Posterior circulation—Vertebral or basilar artery branches supplying the brainstem

Question 8

Oculomotor deficits and/or ataxia with crossed sensory/motor deficits (vascular territory, additional comments)

Answer 8

vascular territory: Posterior circulation—basilar artery

additional comments: Complete basilar artery occlusion—“locked-in syndrome” with intact consciousness but with inability to speak and quadriplegia

Question 9

resting static tremors

Answer 9

These tremors are most prominent at rest and may decrease or disappear with voluntary movement. Illustrated is the common relatively slow, fine pill-rolling tremor of parkinsonism, about 5/sec.

Question 10

postural tremors

Answer 10

These tremors appear when the affected part is actively maintaining a posture. Examples include the fine rapid tremor of hyperthyroidism, the tremors of anxiety and fatigue, and benign essential (and often familial) tremor.

Question 11

intention tremors

Answer 11

Intention tremors, absent at rest, appear with movement and get worse as the limb approaches the target. Seen in disorders affecting the cerebellum or its related tracts, such as multiple sclerosis or stroke.

Question 12

oral-facial dyskinesias

Answer 12

-involuntary movements

Oral–facial dyskinesias are arrhythmic, repetitive, bizarre movements that chiefly involve the face, mouth, jaw, and tongue: grimacing, pursing of the lips, protrusions of the tongue, opening and closing of the mouth, and deviations of the jaw. The limbs and trunk are involved less often. These movements may be a late complication of antipsychotic or antiemetic drugs such as phenothiazines, termed tardive (late) dyskinesias. They also occur in long-standing psychoses, in some older adults, and in some edentulous persons.

Question 13

tics

Answer 13

Tics are brief, repetitive, stereotyped, coordinated movements occurring at irregular intervals. Examples include repetitive winking, grimacing, and shoulder shrugging. Causes include Tourette syndrome and late effects of drugs such as phenothiazines.

Question 14

dystonia

Answer 14

Dystonia causes irregular movements resembling athetosis or tremor. These are often accompanied by abnormal postures that limit voluntary movement and can at times be painful. Examples include writer’s cramp, blephorospasm, and as illustrated, spasmodic torticollis.

Question 15

athetosis

Answer 15

Athetoid movements are slower and more twisting and writhing than choreiform movements and have a larger amplitude. They most commonly involve the face and the distal extremities. Athetosis is often associated with spasticity. Causes include cerebral palsy.

Question 16

chorea

Answer 16

Choreiform movements are brief, rapid, jerky, irregular, and unpredictable. They occur at rest or interrupt normal coordinated movements. Unlike tics, they seldom repeat themselves. The face, head, lower arms, and hands are often involved. Causes include Sydenham chorea (with rheumatic fever) and Huntington disease.

Question 17

Upper motor neuron or corticospinal tract systems - lesion

Answer 17

Increased muscle tone (hypertonia) is rate dependent. Tone increases when passive movement is rapid, and decreases when passive movement is slow. Tone is also greater at the extremes of the movement arc.

During rapid passive movement, initial hypertonia may give way suddenly as the limb relaxes. This spastic “catch” and relaxation is known as “clasp-knife” resistance.

common cause: Stroke, especially late or chronic stage

Question 18

Basal ganglia system- lesion

Answer 18

Increased resistance that persists throughout the movement arc, independent of rate of movement, is called lead-pipe rigidity.

During flexion and extension of the wrist or forearm, a superimposed ratchet-like jerkiness is called cogwheel rigidity and can be due to underlying tremor.

common cause: Parkinsonism

Question 19

Lower motor neuron system at any point from the anterior horn cell to the peripheral nerves, and in cerebellar disease - lesion

Answer 19

Loss of muscle tone (hypotonia) causes the limb to be loose or floppy. The affected limbs may be hyperextensible or even flail-like. Flaccid muscles are often weak.

common cause: Guillain–Barré syndrome; also initial phase of spinal cord injury (spinal shock) or stroke

Question 20

Both hemispheres, usually in the frontal lobes- lesion

Answer 20

Sudden, irregular changes in tone accompany passive range of motion.

Sudden loss of tone that increases the ease of motion is called facilitatory paratonia, or mitgehen (moving with).

Sudden increase in tone making motion more difficult is called oppositional paratonia, or gegenhalten (holding against).

common cause: dementia

Question 21

glasgow coma scale

Answer 21

eye- 1-4
motor- 1-6
verbal- 1-5

total- 3-15
3-8- coma