Neurology: Reflexes and Bladder Control

the concept that the entering dorsal roots carry sensory information and the exiting ventral roots carry motor information

cerebral cortex stimulating or inhibiting the external urethral sphincter valve

relaxation of the urethral sphincter and contraction of destructor muscle in response to increased intravesicle pressure in the bladder

Pelvic-Afferent And efferent parasympathetic nerves, control destructor
Hypogastric-efferent sympathetic nerve,control IUS
Pudendal-somatic , control the EUS

Sacral Micturition center-voiding
Pontine micturition center-guarding/filling
Cortical and subcortical centers-send impulse to EAS

Afferent impulse: myenteric plexus, splachnic nerves
Efferent
: parasympathetic pelvic nerve-contraction of descending colon, relax IAS
and sympathetic hypogastric -relax descending colon,contract IAS
Pudendal nerve-control EAS

the inability to control the bowels, leading to involuntary passage of stool.

Problem expelling stool from rectum

Erection reflexes
Ejaculation reflexes

penis becomes engorged with blood as the vascular spaces in the erectile tissues fill with blood
-spinal parasympathetic reflex

Spinal sympathetic reflex

Ipsilateral loss of light touch, vibration, and position sense below lesion

contralateral loss of pain and temperature (1-2 segments below)

Loss of pain and temperature sensation at c5-c6 dermatomes bilaterally

Ipsilateral spastic paralysis below lesion
Ipsilateral flaccid paralysis at the level of lesion

Bilateral loss of light touch, vibration and position sense

- bilateral LMN symptoms at lesion
- bilateral UMN symptoms below the lesion
-bilateral loss of pain and temperature

total loss of respiratory muscle funcion (need ventilator)

C3,C4,C5 keeps the diaphragm alive

-Bilateral loss of light touch, vibration, position sense
-Bilateral UMNL signs
-Bilateral loss of pain and temperature
-paraplegia

-Bilateral loss of light touch, vibration, position sense
-Bilateral UMNL signs
-Bilateral loss of pain and temperature
-quadriplegia

midbrain

midbrain

Hypertonia
Hyperreflexia
Spastic paralysis
Babinski (Abnormal plantar reflex)
Clonus

Hypotonia
Arreflexia
Flaccid paralysis
Normal plantar reflex
Fasciculation
Atrophy

LMN destroyed-> no impulse reach muscle fibers-> no contraction

Upper motor neurons destroyed ->LMN still can be stimulated by reflex arc->involuntary and spastic

physiologic response that occurs between 30 and 60 minutes after trauma to the spinal cord and can last up to several weeks.

-usually above t6

0-1 day
total flaccid paralysis , loss of descending motor facilitation and loss of all reflexes (including visceral) below the level of injury.
1-3 days
-Return of urogenital reflex
-Inbalanced between more postsynaptic receptors with reduced afferent facilitates spinal reorganisations
2 w-1y
-Sprouting of collaterals from interneurons to re-establish synapses (may cause neuropathic pain)
- Signs of UMNL signs

Loss of sympathetic innervation
Low HR
Vasodilation
Hypotension

This typically occurs with patients suffering a severe SCI at the level of T6 or higher.

Descending inhibitory signals blocked at SCI. Sympathetic response cannot be compensated below level of SCI

After spinal shock
Usually above T6
HPT
Parasympathetic activity above level of injury (flushing of skin, Bradycardia)

lateral ventricles, interventricular foramen (foramen of Monro), 3rd ventricle, cerebral aqueduct( aqueduct of sylvius), 4th ventricle, median (foramen of magendie) and lateral apertures(foramen of luschka), subarachnoid space, arachnoid granulations, dural sinuses, internal jugular vein

Pressure inside brain but outside blood vessels

-Cranial vault is a fixed space.
-3 intracranial components
-Blood
-Brain
-CSF
-Any increase in once component requires a decrease in another.

choroid plexus

Rate of formation=500 ml/day (Mean volume=125-150 ml, renewed =3-4x day)

Choroid epithelial cells actively secrete sodium-> draws water into CSF space

Caused by structural blockage of CSF circulation within the ventricular system (herniations, etc.)

failure of the subarachnoid to absorb CSF

VP shunt

Signs of increased intracranial pressure:
1. hypertension
2. bradycardia
3. irregular respirations

Headache
-worse in upright position
-Visual, auditory and balance problems
-Discharge of ECF through nose/ear

AMPA, NMDA, Kainate (all ionotropic)

Membrane Depolarization (to displace the mg2)

Brain

spinal cord and brain stem

But also co-transmitter in excitatory NMDA synapses

Glutamate

Glutamate by GAD

GABAa (ionotropic) and GABAb (metabotropic)

ionotropic, producing fast, inhibitory effects, post synaptic inhibition (allow Cl- inside)

benzodiazepines and barbiturates

Metabotropic receptor for GABA, increases K+ conductance,inhibit both pre and post synaptic

Serine in mitochondria

Ionic
Permeable to Cl-

rat poison (strychnine)->inability to relax diaphragm

Astrocytes end feet
Pericytes
Endothelium with tight junctions

-Paracellular aqueous pathway-water
-Transcellular lipophilic pathway-lipid soluble agents (O2, ethanol, caffeine,nicotine etc)
-Facilitated diffusion -glucose (GLUT-1), amino acids, nucleosides
-Receptor-mediated transcytosis-Insulin, transferrin
-Adsorptive transcytosis-Albumin, +ve charged object

a) Subfornical organ-Thirst centre
b) Organum Vasculosum of Laminate Terminalis-Osmoreceptor
c)Post. Pituitary-Release Oxytocin
d) Area Postrema-Vomiting Center
e) Subcommisural Organ- (unidentified yet)
f)Pineal body (Melatonin-circadian rhythm)

Oral, rectal, tympanic membrane

Forehead and armpit
Shell temperatures are generally higher than core temperatures.


a. True

True

36.5-37.5

Rise in temperature (0.5 C)

Higher temperature

Conduction and radiation

BMR, voluntary movement, shivering

Prevent sodium depletion as aldosterone reabsorb sodium and produce hypotonic swear

The transfer of energy by electromagnetic waves

Loss the most heat under covered area but the least when walking outside

Loss of heat the least

hypothalamus (preoptic area)

Skin and visceral

Internal blood temperature

Loss (antirise centre)

Body temp maintained through a flexed posture & brown fat..
Beta adrenergic will activate thermogenin hence cause the increase of permeability of inner mitochondria to H+ . Faster substrate oxidation generate more heat compared to atp

Pyrogens sensed by circumventricular organ -> produce prostaglandin ->which raise the hypothalamus set point

reduce fever by opposing the production of prostaglandins by arachidonic acid(cox inhibition

Aspirin and paracetamol

low core temperature <35 C

Low BP

Unconscious

Ventricular fibrillation x

Core temperature >37.5

Circulatory shock

Organ and tissue death

dynamic equilibrium (determining rotary motion of the head)

regulation of the volume and pressure of endolymph, the immune response of the inner ear, and the elimination of endolymphatic waste products by phagocytosis.

Superior (anterior)
Posterior and horizontal (lateral)bb

Perpendicular to each other

30 degrees to horizontal plane

45 degrees from sagittal plane

Epithelium bearing hair cells

gelatinous cap overlying hair cells of the crista ampullaris

Depolarisation

Movement of endolymph

Head rotate->endolymph inertia cause it to lag-> endolymph move in opposite direction from head rotation -> opens K plus channel -> depolarisation
A turn of the head excites the receptors in one ampulla and inhibits receptors in the ampulla on the other side.

A. True

True

horizontal acceleration and right and left head tilt

vertical acceleration and front and back tilt

Contains calcium carbonate

Macula-> dense otoliths lag behind due to inertia->shearing movement->bending of stereoclia

Maintains stable image while allowing head to move
-necessary for vision stabilization

Postural control - maintains balance and head position
Supplies muscles of trunk and lower limb

Provide rapid and sensitive response to head position

Postural unsteadiness

Vertigo

Nystagmus

Fast phase will follow the direction of acceleration

As soon as head rotation stops, nystagmus flips and is opposite the direction of head rotation.

VOR test for nystagmus (involuntary eye movement) induced by irrigating the auditory canal with cold or warm water

Cold
Opposite
Warm
Same

Comatose patient's pons is *NOT functionally intact* - brain herniation

CN 2 (afferent)
CN 3 (efferent)

*Oculocephalic Reflex Test*
Performed by turning head back and forth.

Intact = eyes move conjugately away from direction turning (as if still looking at the examiner rather than fixed straight ahead).

Compromised = Eyes stay fixed midorbit = negative "doll's eyes"

When turning patients head, the eyes go with the direction of the turn

*Brainstem damage*