Exam #1 neurology

neurological history

symptoms (subjective)

neurological exam

signs (objective)

focal

discrete, well defined part of nervous system

diffuse

affecting a functional system

multifocal

multiple focal lesions

focal lesion symptoms/ signs are usually 

unilateral
can cause bilateral symptoms/ signs (ex: midline lesions)

diffuse lesion symptoms/ signs are usually

bilateral
can cause asymmetric symptoms/ signs (ex parkinson)

symptoms

what the patient reports

acute

instanteous → 2 hours

subacute

many hours → 2 months

chronic

many months → years

positive symptoms 

not normally present 

negative symptoms

loss of function

lesion

damage causing a neurological problem

localizing

requires history/ exam + knowledge of neuroanatomy structure/ function

vascular

acute, focal

endocrinological nutritional

subacute (acute, chronic), diffuse

neoplastic

subacute (malignant)/ chronic (benign), focal

degenerative

chronic, diffuse

hyperkalemia etiology

increase intake
increase movement out of cell or decrease movement into cell (tissue catabolism, trauma, metabolic acidosis, decrease insulin effect, b2 receptor blockade, hyperglycemia, intense skeletal muscle contractions)

decrease renal excretion (renal failure, decrease aldosterone effect, damage to adrenal cortex)

hyperkalemia physiological effects

decrease chemical gradients
Ek+ less negative
V rest less negative
increase excitability initially (V rest closer to threshold)
decrease excitability to depolarization blockage (chronic inactivation of voltage-gated Na+ channels)

hyperkalemia clinical findings

• skeletal muscle weakness (diffuse)

• tall, peaked T waves (accelerate repolarization)

• decrease QT interval

• widened QRS interval

• flattened P wave (V gated Na+ channel is inactivated, affects conduction)

hyperkalemia treatment

insulin + glucose (avoid hypoglycemia)

b2 agonist 
resin (binds K+ in GI tract)

K+ wasting diuretics 

calcium gluconate = stabilizes membrane of cardiac cells, decreases arrhythmias  

hypokalemia etiology

decrease intake
increase movement into cells (metabolic alkalosis, increase insulin, b2 agonist)
increase loss from body
increase renal excretion from drugs or excess aldosterone effects

physiological effects of hypokalemia

increase chemical gradient
Ek+ more negative
V rest more negative
decrease excitability (V rest further from threshold)

clinical findings of hypokalemia

skeletal muscle weakness - diffuse
U wave (occurs after T wave)
decrease T wave amplitude
increase QT interval
increase P wave amplitude
acquired nephrogenic DI → impaired urinary concentrating ability (decrease ADH) → polydipsia/ polyuria
decrease B cell insulin secretion → increase plasma glucose

treatment for hypokalemia

give K+
K+ sparring diuretics 

hypercalcemia etiology

increase bone reabsorption
decrease renal excretion 
increase GI reabsorption 

2 most common causes of hypercalcemia

1) primary hyperparathyroidism → increase PTH

2) hypercalcemia of malignancy from secretion of PTHrP

also CKD, hyperparathyroidism

physiological effects of hypercalcemia

decrease activation of V gated Na+ channels (decrease movement of positive charges)
smooth muscle contraction in some places

decrease ADH effect

activation of cardiac K+ channels

clinical findings of hypercalcemia

skeletal muscle weakness - diffuse (due to reduced excitability) 

decrease muscle stretch reflexes (decreased excitability → decreased reflexes)

increase BP, calcium deposition in heart valves, coronary arteries

decrease QT interval

polyuria/ polydipsia/ nephrolithiasis 

constipation/ nausea/ pancreatitis 

anxiety/ depression/ cognitive dysfunction

treatment for hypercalcemia

remove parathyroid adenoma

calcimimetics - stimulate calcium sensitive receptor on parathyroid glands → decrease PTH

calcitonin bisphosphonates → decrease bone reasborption → decreases Ca2+ releases 

furosemide → increase Uca 

hypocalcemia etiology

decrease bone reabsorption

increase Uca

decrease GI absorption

major cause of hypocalcemia

hypoparathyroidism from surgical removal

physiological effects of hypocalcemia

increase activation of voltage gated Na+ channels (increase movement of positive charges)

decrease smooth muscle contraction 

decrease activation of cardiac K+ channels 

clinical effects of hypocalcemia

skeletal muscle/ neurons - neuromuscular excitability

perioral numbness

parasthesia hands/ feet

muscle cramps

increased muscle stretch reflexes

seizures

anxiety/ depression

trosseau sign

chvostek’s sign

hypotension

increased QT interval

arrhythmia

trosseau signs

inflate BP cuff > SBP 3 mins → abnormal spasm from hyperexcitability of neurons

chvostek’s sign

abnormal contraction of ipsilateral face muscle following tappng CNVII just anterior to ear

treatment for hypocalcemia

give Ca2+
vitamin D

PTH 

facilius cuneatus

T6 and above (lateral)

facilius gracilus

through (midline)

lateral coritospinal tract is for

motor system

dorsal column/ medial menicus tract is for

discriminative touch/ proprioception

spinothalamic tract is for

pain/ temperature/ crude touch

1st order soma of dorsal column/ medial lemnicus

DRG

2nd order soma of dorsal column/ medial lemnicus

caudal medulla (nucleus gracilus/ nucleus cuneatus) 

3rd order soma of dorsal column/ medial lemnicus

VPl thalamus 

decussation of dorsal column/ medial lemnicus

caudal medulla
internal arcuate fibers

1st order soma of spinothalamic tract/ spinal lemnicus 

DRG

2nd order soma of spinothalamic tract/ spinal lemnicus 

spinal cord
- dorsal horn

3rd order soma of spinothalamic tract/ spinal lemnicus 

VPl thalamus 

decussation of spinothalamic tract/ spinal lemnicus 

spinal cord (AWC)

cerebral hemispheres are separated by

interhemispheric fissure

frontal lobe

primary motor cortex
frontal eye fields
prefrontal cortex (executive functioning)
broca’s area (language production)
olfactory bulb/ tract

parietal lobe

primary somatosensory cortex

temporal lobe

primary auditory cortex
wernicke’s area (language comprehension)

occipital lobe

primary visual cortex

hippocampus

important for memory, medial temporal lobe

thalamus

consists of several nuclei involved in somatosensory, auditory, vision, motor feedback, memory, consciousness, NOT voluntary movement

cerebellum

smooths and coordinates voluntary movement of the extremities 

hypothalamus

small group of nuclei involved in maintenance of hemostasis and plays a major role in regulating several endocrine organs 

somatotopic representation

leg (medial)
arm, face (lateral)

midbrain consists of

tegmentum, substantia nigra, crus cerebri

tegmentum

sensory information, cranial nerve nucleus

substantia nigra

dopaminergic neurons/ motor feedback

crus cerebri

caries motor neurons

pons consists of 

tegmentum and basis pontis

medulla consists of

tegmentum and pyramid

ventral

motor information (UMNs traveling down)

dorsal

sensory (traveling up)

arms

c5-t1

chest/ thorax

t2-t12

legs/ le

l1-s2

upper motor neurons

frontal lobe

lower motor neurons

brainstem, spinal cord

neuromuscular junction

ach

skeletal muscle

nm cholinergic

motor system path

crus cerebri → basis pontis → pyramids (decussation) → lateral corticospinal tract

lower motor neurons that control forehead are controlled by _ UMNS

2

CNIII

oculomotor nerve
exits the midbrain through the interpendicular fossa

facial motor nucleus is found in

caudal pontine tegmentum

CNVI

abducens nerve
exits the caudal pons ventrally at the pontomedullary junction

CNXII

hypoglossal nerve

exits the medulla ventrally in between the. olive and pyramid