First Aid Neurology Part 4

Front 1

Describe hydrocephalus

Back 1

-Accumulation of excess CSF in ventricular system leads to increased intracranial pressure
-This causes ventricular dilation
-There is a clinical triad of dementia, gait problems, and urinary incontinence, "wet, wobbly, and wacky"

Front 2

Describe normal pressure hydrocephalus

Back 2

-Communicating hydrocephalus
-Caused by impaired absorption of CSF by arachnoid granulations (e.g., arachnoid adhesions post-meningitis)

Front 3

Describe obstructive hydrocephalus

Back 3

-Non-communicating
-Caused by structural blockage of CSF circulation within the ventricular system (e.g., stenosis of the aqueduct of Sylvius)

Front 4

Describe hydrocephalus ex vacuo

Back 4

-Appearance of increased CSF in atrophy
-Intracranial pressure normal, triad not seen

Front 5

How many spinal nerves are there?

Back 5

-31 nerves altogether
-8 cervical
-12 thoracic
-5 lumbar
-5 sacral
-1 coccygeal

Front 6

Describe how the spinal nerves exit

Back 6

-Nerves C1-C7 exit via intervertebral foramina and the corresponding vertebra
-All other nerves exit below

Front 7

Describe vertebral disk herniations

Back 7

-Nucleus pulposus herniates through annulus fibrosus
-Usually occurs between L5 and S1

Front 8

Describe the lower extent of the spinal cord

Back 8

-In adults, spinal cord extends to lower border of L1-L2
-Subarachnoid space extends to lower border of S2

Front 9

Describe lumbar punctures

Back 9

-Usually performed in L3-L4 or L4-L5 interspaces (at the level of the iliac crests, at level of cauda equina
-To keep the cord alive, keep the spinal needle between L3 and L5
-CSF obtained from lumbar subarachnoid space

Front 10

What order are structures pieces in during a lumbar puncture?

Back 10

1. Skin/superficial fascia
2. Ligaments (supraspinous, interspinous, ligamentum flavum)
3, Epidural space
4. Dura mater
5. Subdural space
6. Arachnoid
7. Subarachnoid space - CSF

Front 11

Describe the function, 1st order neuron, 1st synapse, 2nd order neuron, 2nd synapse, and 3rd order neuron of the dorsal column-medial lemniscal pathway

Back 11

Function: Ascending pressure, vibration, touch and proprioceptive sensation

1st order neuron: Sensory nerve ending to cell body in dorsal root ganglion to enter spinal cord, ascends ipsilaterally in dorsal column

Synapse 1: Ipsilateral nucleus cuneatus or gracilis (medulla)

2nd-order neuron: Decussates in medulla to ascend contralaterally in medial lemniscus

Synapse 2: VPL of thalamus

3rd order neuron: Sensory cortex

Front 12

Describe the function, 1st order neuron, 1st synapse, 2nd order neuron, 2nd synapse, and 3rd order neuron of the spinothalamic tract

Back 12

Function: ascending pain and temperature sensation

1st order neuron: Sensory nerve ending (A-delta and C fibers) (cell body in dorsal root ganglion) to enter spinal cord

Synapse 1: Ipsilateral gray matter (spinal cord)

2nd order neuron: Decussates at anterior white commissure to ascend contralaterally

2nd synapse: VPL of thalamus

3rd order neuron: Sensory cortex

Front 13

Describe the function, 1st order neuron, 1st synapse, 2nd order neuron, 2nd synapse, and 3rd order neuron of the lateral cortical tract

Back 13

Function: Descending voluntary movement of contralateral limbs

1st order neuron: Upper motor neuron: cell body in primary motor cortex then descends ipsilaterally (through internal capsule) until decussating at caudal medulla (pyramidal decussation) then descends contralaterally

Synapse 1: Cell body of anterior horn (spinal cord)

2nd order neuron: Lower motor neuron: Leaves spinal cord

Synapse 2: Neuromuscular junction

Front 14

What are the motor neuron signs of a upper motor neuron lesion?

Back 14

Weakness: +
Atrophy: -
Fasciculation: -
Reflexes: increased
Tone: increased
Babinski: +
Spastic paralysis: +

Upper MN = everything up (tone, DTRs, toes)

Front 15

What are the motor neuron signs of a lower motor neuron lesion?

Back 15

Weakness: +
Atrophy: +
Fasciculation: +
Reflexes: decreased
Tone: decreased
Babinski: -
Spastic paralysis: -

Lower MN = Everything lowered (less muscle mass, decreased muscle tone, decreased reflexes, downgoing toes)

Front 16

Describe the Babinski in infants

Back 16

Upgoing Babinski is normal in infants

Front 17

What are fasciculations?

Back 17

Muscle twitching

Front 18

Describe poliomyelitis

Back 18

-Caused by poliovirus
-Virus transmitted by fecal-oral route
-Replicates in the oropharyx and small intestine before spreading through the bloodstream to the CNS, where it leads to the destruction of cell sin the anterior horn of the spinal cord, leading in turn to LMN destruction

Front 19

What are the symptoms of poliomyelitis?

Back 19

-Malaise
-Headache
-Fever
-Nausea
-Abdominal pain
-Sore throat
-Signs of LMN lesions:
-Muscle weakness and atrophy
-Fasciculations
-Fibrillation
-Hyporeflexia

Front 20

What are the clinical findings of poliomyelitis?

Back 20

-CSF with lymphocytic pleocytosis with slight elevation of protein (with no change in CSF glucose).
-Virus recovered from stool or throat

Front 21

Describe Werdnig-Hoffman disease

Back 21

-Also known as infantile spinal muscular atrophy
-Autosomal-recessive inheritance
-Presents at birth as a "floppy baby", tongue fasciculations
-Median age of death 7 months
-Associated with degeneration of anterior horns.
-LMN involvement only

Front 22

Describe amyotrophic lateral sclerosis

Back 22

-Associated with both LMN and UMN signs
-No sensory, cognitive, or oculomotor deficits
-Can be caused by defect in superoxide dismutase 1 (SOD1), betel nut ingestion
-Commonly known as Lou Gehrig's disease

Front 23

Describe Tabes dorsalis

Back 23

-Degeneration of dorsal columns and dorsal roots due to tertiary syphilis
-Results in impaired proprioception and locomotor ataxia
-Associated with Charcot's joint, shooting (lighting) pain, Argyll Robertson pupils (reactive to accommodation but not to light), and absence of DTRs

Front 24

What are Argyll Robertson pupils?

Back 24

-Pupils that are reactive to accommodation but not to light
-Known as "prostitute;s pupils" because they accommodate but do not react

Front 25

Describe Friedreich's ataxia

Back 25

-Autosomal-recessive trinucleotide repeat disorder (GAA; frataxin gene)
-Leads to impairment in mitochondrial functioning
-Staggering gait, frequent falling, nystagmus, dysarthria, hypertrophic cardiomyopathy
-Presents in childhood with kyphoscoliosis

Front 26

Describe Brown-Sequard syndrome

Back 26

-Hemisection of spinal cord
-Findings:
1. Ipsilateral UMN signs (corticospinal tract) below lesion
2. Ipsilateral loss of tactile, vibration, proprioception, sense (dorsal column) below lesion
3. Contralateral pain and temperature loss (spinothalamic tract) below lesion
4. Ipsilateral loss of all sensation at level of lesion
5. LMN signs (e.g., flacid paralysis) at level of lesion

If lesion occurs above T1, presents with Horner's syndrome

Front 27

Describe Horner's syndrome

Back 27

Sympathectomy of face
1. Ptosis (slight drooping of eyelid)
2. Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face
3. Miosis (pupil constriction

Associated with lesion of spinal cord above T1 (e.g., Pancoast's tumor, Brown-Sequard syndrome [cord hemisection], late-stage syringomyelia)

Front 28

Describe the pathway where lesions result in Horner's syndrome

Back 28

-3-neuron oculosympathetic pathway projects from the hypothalamus to the intermediolateral column of the spinal cord
-Then to the superior cervical (sympathetic) ganglion
-And finally to the pupil, the smooth muscle of the eyelids, and the sweat glands of the forehead and face

Front 29

What landmark is important for pudendal nerve block?

Back 29

-For relieving pain of pregnancy
-Ischial spine

Front 30

What landmark is important for the appendix?

Back 30

2/3 of the way from the umbilicus to the anterior superior spin (McBurney's point)

Front 31

What landmark is important for lumbar punctures?

Back 31

Iliac crest