Neurology

Front 1

Components of nervous system

Back 1

UMN: lesions will cause imperfect movement
1. Basal Ganglia
2. Cerebellum
3. Sensory
LMN: lesions will cause weakness
1. NMJ

Front 2

Pathway of UMN of left leg

Back 2

1. RIGHT Motor Cortex
2. R internal capsule
3. Crosses to LEFT medulla
4. L spine
5. LMN

Front 3

Basal Ganglion function is ipsilateral or contralateral?

Cerebellar control?

Back 3

contralateral

Ipsilateral

Front 4

Ascending pathway of Pain and Temperature sensation

Back 4

1. peripheral nerves
2. dorsal root ganglion
3. crosses and ascends contralateral lateral column
4. up to contralateral thalamus
5. sensory cortex

Front 5

Ascending pathway of Position Sense

Back 5

1. Peripheral nerves
2. Dorsal root ganglion
3. ipsilateral Gracille or cuneate nucleus
4. Crosses at medulla
5. up to contralateral thalamus
6. sensory cortex

Front 6

The axons of the upper motor neurones in the precentral motor cortex funnel down to descend in the_______ part of the internal capsule

Back 6

anterior

Front 7

The axons of the 3rd sensory neurone in the thalamus radiate out through the ________ part of the internal capsule to reach the postcentral sensory cortex.

Back 7

posterior

Front 8

Characterics of upper motor lesions

Back 8

no wasting;
increased tone of clasp-knife type;
weakness most evident in anti-gravity muscles;
increased reflexes and clonus;
extensor plantar responses.

Front 9

lesion of motor homunculus

Back 9

Contralateral monoparesis

A lesion situated peripherally in
the cerebral hemisphere, i.e. involving part of the motor homunculus only, produces weakness of part of the contralateral side of the body, e.g. the contralateral leg. If the lesion also involves the adjacent sensory homunculus in the postcentral gyrus, there may be some sensory loss in the same part of the body.

Front 10

lesion of internal capsule

Back 10

Contralateral hemiparesis

Lesions situated deep in the cerebral hemisphere, in the region of the internal capsule, are much more likely to produce weakness of the whole of the contralateral side of the body, face, arm and leg. Because of the funnelling of fibre pathways in the region of the internal capsule, such lesions commonly produce significant contralateral sensory loss (hemianaesthesia) and visual loss (homonymous hemianopia), in addition to the hemiparesis.

Front 11

unilateral lesion in the spinal cord below the level of the neck (thoracic lesion)

Back 11

Ipsilateral monoparesis

A unilateral lesion in the spinal cord below the level of the neck produces upper motor neurone weakness in one leg. There may be posterior column (position sense) sensory loss in the same leg, and spinothalamic (pain and
temperature) sensory loss in the
contralateral leg. This is known as dissociated sensory loss, and the whole picture is sometimes referred to as the Brown-Séquard syndrome

Front 12

unilateral high cervical cord lesion

Back 12

Ipsilateral hemiparesis

A unilateral high cervical cord lesion will produce a hemiparesis similar to that which is caused by a contralateral cerebral hemisphere lesion, except that the face cannot be involved in the hemiparesis, vision will be normal, and the same dissociation of sensory loss (referred to above) may be found below the level of the lesion

Front 13

Characteristics of lower motor neurone lesions

Back 13

• wasting;
• fasciculation;
• decreased tone (i.e. flaccidity);
• weakness;
• decreased or absent reflexes;
• flexor or absent plantar responses.

Front 14

Characteristics of NMJ dz

Back 14

Think myasthenia gravis:
• no wasting/tone normal/reflexes normal
• weakness/fatiguability
• positive response to anticholinesterase.

Front 15

Characteristics of primary muscle disease

Back 15

• wasting;
• no fasciculation;
• weakness/Trendelenburg sign
• tone normal or reduced;
• reflexes normal or reduced.

Front 16

Two main syndromes of basal ganglia dsfnx

Back 16

1. Parkinson’s disease:
• tremor at rest;
• increased tone;
• bradykinesia;
• flexed posture.

2. Involuntary movements:
• involuntary movements at rest and during action;
• tone increased, normal or reduced;
• normal speed of movement;
• all sorts of postural abnormalities.

NO WEAKNESS IN EITHER

Front 17

Cerebellar lesion

Back 17

1. Incoordination of muscle activity:
• in the head: nystagmus, dysarthria;
• in the arms: finger–nose ataxia, kinetic tremor, difficulty with rapid alternating movements (dysdiadochokinesia);
• in the legs: heel–knee–shin ataxia, gait ataxia, falls.

2. There is no weakness. (Alcohol in large doses impairs cerebellar function. Intoxicated people show all the features of muscular incoordination mentioned above, but may be very strong.)

3. In a unilateral cerebellar lesion, the neurological deficit is ipsilateral to the side of the lesion. A patient complaining of malfunction of the left leg due to a left cerebellar lesion would have heel–knee–shin ataxia most marked in the left leg, and gait ataxia with deviation to the left. There might also be left arm cerebellar signs, and nystagmus most marked looking to the left.

Front 18

Three main clinical syndromes where sensory loss
may play an important role in impairing movement and
function

Back 18

Cerebral hemisphere lesions:
impaired accurate movements of the contralateral limbs because central registration of limb position is lost.

Loss of proprioceptive sense in the legs and feet may occur as a result of SPINAL CORD DISEASE

PERIPHERAL NEUROPATHY

Front 19

Ischemic Stroke Management:

Back 19

1. Confirm dx with CT
2. Thrombolysis w/in 3 hrs
3. Control BP with thiazides/ACEI if SBP>200
4. CBC, ESR, Carotid duplex, lipids, EKG/CXR for cardiac etiologies, ECHO if u suspect embolism
5. ASA, plavix, or ASA/aggrenox; statin, warfarin if afib
6. Cerebral edema 3-4d post stroke from inc ICP so elevate head/hypervent/mannitol

Front 20

Management of Subarachnoid Bleed

Back 20

1. CT and then LP if neg
2. Nifedipine minimizes cerebral infarct.
3. Correct electrolytes
4. Neurosurg consult to try to clip aneurism
5. Rehab

Front 21

Management of Intracerebral hemorrhage

Back 21

1. CT to confirm dx
2. Control BP
3. Reduce ICP with mannitol/hypervent/etc

Front 22

Cranial nerves: why are I, II, XI special?

Back 22

Cranial nerves 1, 2 and 11 are a little different from the others. Nerves 1 and 2 are highly specialized extensions of the brain, for smell and sight, in the anterior cranial fossa and suprasellar region. Nerve 11 largely originates from the cervical spinal cord, rises into the posterior fossa only to exit it again very quickly, to supply muscles of the neck and shoulder.

Front 23

Causes of olfactory nerve defects?
MC cause of decreased smell?

Back 23

CN I lesions are rare but include:
-Head injx either involving fx in the anterior fossa floor, or as a result of damage to the nerves on the anterior fossa floor at the time of impact of the head injury.
-Idiopathic anosmia
-Tumor arising from the floor of the anterior fossa

MC cause of decreased smell is infective or allergic edema of the nasal mucosa

Front 24

Monocular blindness
(XX) (__)

Back 24

prodromal phase of migraine
thrombo-embolism in the ophthalmic artery from the ICA

Front 25

Bitemporal hemianopia
(x_) (_x)

Back 25

optic chiasm compression, usually by pituitary adenomas, but rarely: craniopharyngiomas, meningiomas
and large internal carotid artery aneurysms are alternatives

Front 26

Homonymous hemianopia
(x_) (x_)

Back 26

posterior cerebral artery occlusion and infarction of the occipital cortex is the commonest cerebral hemisphere lesion.
Infarct or hematoma in the region of the internal capsule may cause a contralateral homonymous hemianopia, due to involvement of optic tract fibers in the posterior limb of the internal capsule.