Patho - Neurological System Flashcards
Describe how the nervous system is divided STRUCTURALLY and its components.
1) Central Nervous System (CNS)
- brain (enclosed within cranial vault)
- spinal cord (enclosed within vertebrae)
2) Peripheral Nervous System (PNS)
- cranial nerves
- spinal nerves
- ^their respective ganglia
- Peripheraly nerve pathways differentiated into:
- afferent pathways (ascending pathways): carry sensory impulses towards CNS
- efferent pathways (descending pathways): carry motor impulses and innervate skeletal muscle/effector organs (away from CNS)
Describe how the peripheral nervous system is divided FUNCTIONALLY.
1) Somatic NS - has motor and sensory pathways that regulate voluntary motor control (i.e. skeletal muscle)
2) Autonomic NS - motor and sensory pathways involved with regulating internal environment (viscera) via involuntary control or organ systems; located in both CNS and PNS
- further divided into:
- sympathetic - responds to stress by mobilizing energy stores, prepares body for defense
- parasympathetic - conserves energy and body’s resources
- both systems function at the same time more or less
Define: effector organs
organs that are innervated by specific components of the NS
What are the two types of cells that make up nervous tissue? Describe what they are and their function in the nervous system.
Neurons: primary cell of NS; electrically excitable cell and transmits information
Non-neuronal neuroglial cells: provides structural support, protection, nutrition for neurons, facilitate neurotransmission
- in CNS: astrocytes, microglia, oligodendrocytes
- in PNS: Schwann cells (neurilemma), satellite cells (a type of Schwann cell)
Structure and Function of neurons
Structure: varies throughout the nervous system (adapted to perform specialized functions)
- three components:
- Soma: cell body (mostly located within CNS and densely packed called nuclei; in PNS, they are in dense groups called ganglia)
- Dendrites: thin branching fibers of the cell; receptive portion of neuron - carry nerve impulses toward cell body
-
Axons: long conductive projections, carry nerve impulses away from cell body
- usually one axon per neuron
Function: detect environmental changes, initiate body responses to maintain dynamic steady state
Cellular components of a neuron
composed of:
- microtubules: transport substances within cell
- neurofibrils: very thin supportive fibers extending throughout neuron
- microfilamnes: transport of cellular produces
- Nissl substances: ER and ribosomes; protein synthesis
Fuel source for neuron
predominantly glucose (without need for insulin for glucose uptake)
Definition: Axon hillock
- cone-shaped process where axon leaves the cell body (i.e. initial segment of axon)
- first part of axon hillock has lowest threshold for stimulation (action potentials begin here)
Axons are wrapped in what material, and what purpose does this serve?
myelin sheath membrane (segmented layer of lipid material called myelin)
insulating substance that speeds impulse propagation (allows action potential to leap between segments rather than flowing along entire axon length = increased velocity)
Definition: Nodes of Ranvier
- periodic gaps in the myelin sheath
- allows for nutrient exchange at these nodes (because you can’t along the myelin sheath) and for axons to branch (forming axon collaterals)
Myelin is produced by what?
In the CNS: produced by oligodendrocytes
In the PNS: produced by Schwann cells
Axons end with what structure?
Telodendria - forms the presynaptic vesicles (synaptic knobs) for neurotranmission
Divergence vs. Convergence (in the context of neurons)
Divergence: ability of branching axons to influence many different neurons
Convergences: branches of various numbers of neurons “converge” on and influence a single neuron
Define Saltatory conduction
describes the way an electrical impulse (flow of ions) skips from node to node down the full length of an axon allowing for faster conduction of an action potential rather than travelling down entire length of axon
Conduction velocity depends on what factors?
1) Myelin coating: presence of myelin = increased velocity
2) Axon diameter: larger axons transmit impulses at a faster rate
Neurons are structurally classified based on number of processes/projections extending from the cell body. What are the four types of neuron configuration/cell types?
1) Unipolar: have one process/projection that branches shortly after leaving cell body (ex. in retina)
2) Pseudounipolar: one axon process and one dendritic process but both fused to each other near cell body; dendritic portion extends away from CNS and axon portion projects into the CNS (ex. sensory neurons in cranial and spinal nerves)
3) Bipolar: have two distinct processes (one axon, one dendrite) arising from cell body (ex. connecting rods and cones in retina)
4) Multipolar: most common; multiple processes with extensive branching (ex. motor neurons)
How are neurons functionally classified?
1) Sensory: afferent, mostly pseudounipolar - carry impulses from peripheral sensory receptors to CNS
2) Associational (aka interneurons): multipolar - transmits impulses from neuron to neuron (sensory to motor neurons); solely located in the CNS
3) Motor: efferent, multipolar - transmit impulses away from CNS to an effector (skeletal muscle or organ)
In skeletal muscle, the end processes of the neuron form a ________________.
neuromuscular (myoneural) junction - basically where neuron meets muscle
In a synapse, the space between the two neurons is called:
synaptic cleft
Neuroglia (i.e. nonneuronal cells) comprise ~ _____ the total brain and spinal cord volume, and are ___ times more numerous than neurons.
half; 5-10x
Function of astrocytes
contribute to synaptic function in CNS
- surround blood vessels & fill spaces between neurons: form specialized contacts between neuronal surfaces and blood vessels
-
contribute to synaptic function in CNS
- provide rapid transport for nutrients and metabolites
- essential component of the blood-brain barrier
- scar forming cells of the CNS (involved with seizures)
- assist in processing information and memory storage
Function of oligodendroglia/oligodendocytes
form myelin sheaths within CNS
Function of ependymal cells
line the CSF-filled cavities (ventricles and choroid plexuses) of the CNS
Function of microglia
remove debris (phagocytosis) in the CNS
Function of Schwann cells
form myelin sheath around axons and direct axonal regrowth and functional recovery in the PNS
Function of non-myelinating Schwann cells
provide metabolic support
True or false. Mature nerve cells do not divide therefore injury can cause permanent loss of function
True
What is Wallerian degeneration? Describe what happens in this process.
What it is: degeneration of a nerve fiber in the distal axon after by injury or disease
What happens:
- 1) swelling in the portion of the axon DISTAL to the cut
- 2) neurofilaments hypertrophy
- 3) myelin sheath shrinks and disintegrates
- 4) axon degenerates and disappears
myelin sheaths re-form into Schwann cells that align in a column between severed part of axon and effector organ
Describe what happens during injury to the proximal end of the axon.
How about injury to the cell body?
- in the proximal end of the injury, changes similar to Wallerian degeneration occur but only up to the next node of Ranvier
- cell body swells and dies via chromatolysis (dispersing Nissl substance) or apoptosis
What happens during the repair process of nerve injury ?
- during repair: increased protein synthesis & mitochondrial activity
- new terminal sprouts project from proximal end and may enter remaining Schwann cell pathway (~7-14 days after injury)
- this is limited to myelinated fibers and generally occurs only in the PNS
- regeneration gets harder once more scar formation occurs, and is limited depending on the nature of the myelin formed by the oligodendrocyte, type of injury, inflammation, and location of injury
Which of the follow nerve injuries in each set would have greater chances of regeneration?
a) injury closer to cell body vs injury further away from cell body
b) crushing injury vs cut injury
c) peripheral nerves injured near spinal cord vs further away from spinal cord
a) injury further from cell body - the closer the injury to the cell body, the more likely nerve cell will die, not regenerate
b) crushing injury - crush injuries sometimes fulley recovery, whereas cut nerves form connective tissue scars that block/slow regeneration of axonal branches
c) peripheral nerves injured further away from spinal cord - if injury to the nerve is close to the spinal cord, it’s slow and poor recovery because super long distance between cell body and where the axon terminates (like in the arms and legs)
How are electrical and chemical impulses generated and conducted by neurons?
By selectively changing electrical potential of the plasma membrane and influencing the release of neurotransmitters
All-or-none response
type of response where the neuron either fires or it doesn’t at all (there is no partial response); as long as the stimulus is strong enough, the membrane will be excited if it reaches the threshold potential
otherwise there is no response if it is sub-threshold
Presynaptic vs postsynaptic neurons
presynaptic neurons: neurons that relay a nerve impulse towards the synapse
post-synaptic neurons: neurons that relay a nerve impulse away from the synapse
In a presynaptic neuron, the nerve impulse reaches the vesicles where NTs are stored in what structure?
synaptic bouton
Neuroplasticity
aka synaptic plasticity - the ability for brain synapses to change in strength and number throughout lift (basically the ability of the brain to adapt to new conditions via re-organizing neural pathways and forming new synapses)
allows recovery from injury
What are neurotransmitters (NTs) and where are they localized?
chemicals synthesized in the neuron and localized in he presynaptic terminal (synaptic bouton)
Describe where the following NTs are usually located and whether they are excitatory or inhibitory (or both).
a) ACh
b) Norepinephrine
c) Serotonin
d) Dopamine
e) Histamine
a) ACh - throughout brain, spinal cord, NMJ in skeletal muscle, ANS synapses; excitatory OR inhibitory
b) Norepinephrine - throughout brain, spinal cord, in some ANS synapses; Excitatory OR inhibitory
c) Serotonin - many areas of brain and spinal cord; inhibitory
d) Dopamine - some areas of brain and ANS synapses; excitatory
e) Histamine - posterior hypothalamus; excitatory (H1 and H2 receptors) AND inhibitory (H3 receptors)
Describe where the following NTs are usually located and whether they are excitatory or inhibitory (or both).
a) GABA
b) Glycine
c) Glutamate and Aspartate
d) Endorphins and Enkephalins
e) Substance P
f) Vasoactive Intestinal peptide
a) GABA - most neurons in CNS; post-synaptic inhibition in brain
b) Glycine - spinal cord; post-synaptic inhibition in spinal cord
c) Glutamate and Aspartate - brain and spinal cord; excitatory
d) Endorphins and Enkephalins - throughout CNS and PNS; inhibitory
e) Substance P: spinal cord, brain, pain sensory neurons, GI tract; excitatory
f) Vasoactive Intestinal peptide (VIP) - GI tract; excitatory
After a NT binds to the receptors on the post-synaptic neuron, depending on the NTs two things can happen:
excitatory postsynaptic potentials (EPSPs)
inhibitory postsynaptic potentials (IPSPs)
Explain what these terms mean.
Excitatory postsynaptic potentials (EPSPs): post-synaptic neuron is depolarized (i.e. excited); If EPSP reaches threshold potential then an action potential (AP) is initiated
Inhibitory postsynaptic potentials (IPSPs): post-synaptic neuron is hyperpolarized (i.e. inhibited); membrane is less likely to reach threshold potential so AP is inhibited
Temporal summation vs spatial summation
Temporal summation: the effects of successive rapid impulses received from a single neuron at the same synapse
Spatial summation: combined effects of impulses from multiple neurons onto a single neuron at the same time (together, they release enough NTs to exceed threshold potential and an AP occurs)
What is facilitation when referring to membrane potentials?
refers to the effect of EPSP on membrane potential (i.e. plasma membrane is “facilitated” when summation brings it closer to threshold potential which reduces the amount of stimulus needed for an AP to occur)
How much does the brain weigh, and how much of the total cardiac output (in % and in ml) does it receive?
3lbs; receives 15-20% of total cardiac output
800-1000ml of blood flow/min
What are the three major structural divisions of the brain?
1) forebrain (prosencephalon - telencephalon & diencephalon)
2) midbrain (mesencephalon)
3) hindbrain (rhombencephalon - cerebellum, pons, and medulla)
What is the brainstem made up of and what structures does the brainstem connect to?
midbrain
medulla
pons
connects: brain hemispheres, cerebellum, and spinal cord
The largest part of the brain is _______ and contains two types of matter which are ______ and ______ matter.
cerebrum; gray & white
A collection of nerve cell bodies (nuclei) in the brainstem makes up the ____________. What is the function of this structure?
reticular formation
Function:
- connects brainstem to cortex
- controls vital reflexes (CV function and resp)
- essential for maintaining wakefulness and attention
- some function in balance and posture
The reticular activating system (RAS) is comprised of:
nuclei in reticular formation
fibers that conduct sensory information to the nuclei
fibers that conduct from nuclei to cerebral cortex
The forebrain (pronsencephalon) is split up into two secondary vesicles, _______________ and _____________. What are the structures in each of these secondary vesicles?
1) Telencephalon: cerebral hemispheres, cerebral cortex, basal ganglia
2) Diencephalon: epithalamus, thalamus, hypothalamus, subthalamus
Structures in the midbrain
1) Tegmentum - floor of midbrain - composed of red nucleus, substantia nigra, and basis pedenculi
* cerebral peduncles - tegmentum and basis pedunculi
2) corpora quadrigemina - located on the tectum (celing of midbrain) - composed of two pairs of each superior and inferior colliculi
Structures in the hindbrain (rhombencephalon)
1) Metencephalon - cerebellum, pons
2) Myelencephalon - medulla oblongata
Define the following terms:
Gyri (gyrus)
Sulci (Sulcus)
Fissures
Gyri (gyrus): ridges/convolutions on the surface of the cerebral cortex
Sulci (Sulcus): grooves in between gyri
Fissures: deeper grooves in between gyri
Composition of gray matter vs white matter
Gray matter: neuron cell bodies (outer layer)
White matter: myelinated nerve fibers (lies beneath cerebral cortex)
Longitudinal fissure
deep groove that separates the two cerebral hemispheres
The posterior margin (border) of the frontal lobe is on the ____________, and the inferior margin of the frontal lobe is on the _______________.
posterior border: Central Sulcus (Fissure of Rolando)
inferior border: Lateral Sulcus (Sylvian fissure, lateral fissure)
Function of prefrontal area
- goal-oriented behaviour (e.g. ability to concentrate)
- ST or recall memory
- elaboration of thought
- inhibition of limbic areas of CNS
Function of premotor area (Brodmann area 6)
programming motor movements
also contains the cell bodies that make up part of the basal ganglia system
The frontal eye fields in the frontal lobe area also known as ____________. They are involved with what function(s)?
Brodmann area 8 (lower portion); involved with controlling eye movements
The primary motor area is also known as __________ and is located where? Describe its general function(s).
- aka Brodmann area 4
- located along the precentral gyrus in the frontal lobe
- forms the primary voluntary motor area (organized into a homunculus) - Function: generate signals to direct the movement of the body
- means that electrical stimulation over specific areas in this cortex cause specific muscle movements
Pyramidal system
two-neuron system that are comprised of corticobulbar tract and corticospinal tracts
- corticobulbar tract: synapses in the brainstem and provides voluntary control of muscles in head and neck
-
corticospinal tracts: originate in precentral gyrus (decussate in medulla oblongata), descend into spinal cord, provide voluntary control of muscles throughout the body
- has the same somatotopic organization as the body
Contralateral control
phenomenon where cerebral impulses control function on the opposite side of the body
Broca speech area
Brodmann area #, Location and Function
- Brodmann areas 44, 45
- Location: on the inferior frontal gyrus (FRONTAL LOBE); usually on L hemisphere
- Function: motor aspects of speech (speech production)
Parietal Lobe
Location, function
- Location: see photo - borders: central sulcus, parietoccipital sulcus, & lateral sulcus
- Function: somatic sensory input (along postcentral gyrus) - storing, analyzing, and interpreting sensory stimuli
Occipital Lobe
Location and Function
- Location: behind parietoccipital sulcus, superior to cerebellum (see photo)
-
Function: primary visual cortex (Brodmann area 17)
- receives visual input from retinas
- Visual association (Brodmann areas 18, 19)
Communication between motor and sensory areas in the cerebral cortex are accomplished through what structures?
association fibers
Temporal Lobe
Location, Structures, and Function
- Location: inferior to lateral fissure
- Structure: composed of superior, middle, and inferior temporal gyri
-
Function:
- primary auditory cortex (Brodmann area 41) and related association area (Brodmann area 42)
- Wernicke’s area: sensory speech area - receiving and interpreting speech
- also involved in memory consolidation and smell
Insula (Insular lobe)
Location and Function
- Location: hidden in lateral sulci between temporal and fronal lobes of each hemisphere
- Function: processes sensory and emotional information and routes the info to other areas of the brain
The two cerebral hemispheres are connected by a mass of white matter pathways collectively known as _________. What is the importance of this structure?
corpus callosum (transverse or commissural fibers)
lies beneath longitudinal fissure; connects the hemispheres through sensory and motor contralateral projections of axons that is needed in coordinating activities between the hemispheres
Basal ganglia system - what is this system comprised of and what is the main function of the basal ganglia system?
Structures: caudate nucleus, putamen, globus pallidus
- putamen x globus pallidus - lentiform nucleus (shaped like a lentil)
- caudate nucleus x putamen - striatum
Other structures: substantia nigra, nucleus accumbens, subthalamic nucleus
Function: involved with voluntary movement, and cognitive and emotional functions (i.e. dopamine and pleasure/reward functions)
Substantia nigra synthesizes what neutrotransmitter that contributes to pleasure and reward functions?
dopamine
What is the internal capsule
thick layer of white matter that carries information (sensory and motor pathways) to and from cerebral cortex, and between caudate and lentiform nuclei
Extrapyramidal system - what is it comprised of and what is its function(s)?
Structures: basal ganglia + interconnections with thalamus, premotor cortex, red nucleus, reticular formation, and spinal cord
Function: motor system network responsible for involuntary control and modulation of muscles (reflexes and movement, stabilizing effect on motor control)
Limbic system
Location, Structure and Function
Location: between telencephalon and diencephalon, surrounds corpus callosum
Structure: composed of amygdala, hippocampus, fornix, hypothalamus, and related autonomic nuclei
Function: mediates emotions, LT memory, primitive behavioural responses, visceral reaction to emotion, motivation, mood, feeding behaviours, biologic rhythms, and smell
- just remember 5 F’s: feeding (hunger/satiety); forgetting (memory); fighting (emotional response), family (sexual reproduction/maternal instincts), fornicating
Describe the structures that the diencephalon is comprised of and their respective locations and functions.
1) Epithalamus: roof of third ventricle; the most superior portion of the diencephalon ⇒ controls vital functions and visceral activities (closely associated with limbic system)
2) Thalamus: borders and surrounds third ventricle ⇒ integrating center for impulses that head to cerebral cortex & relay center for info from basal ganglia and cerebellum to motor areas
3) Hypothalamus: forms base of diencephalon
- maintains constant internal environment
- implement behavioural patterns
- influences body via endocrine system & neural pathways
4) Subthalamus: flanks the hypothalamus laterally ⇒ important for motor activities
Functions of superior colliculi and inferior colliculi
Superior colliculi: involved with voluntary and involuntary visual motor movements (tracking moving objects)
Inferior colliculi: motor activities affecting auditory system (i.e. positioning head to improve hearing)
Input and output of the red nucleus
receives ascending sensory info form cerebellum
projects rubrospinal tract (motor pathway) to cervical spinal cord
Basis pedunculi composition
made up of efferent fibers of cortocospinal, corticobulbar, and corticopontocerebellar tracts
What is the cerebral aqueduct (aqeduct of Sylvius)
The cerebral aqueduct is a channel that connects the third ventricle with the fourth ventricle and allows cerebrospinal fluid to pass between them.
Cerebellum
Structure and Function
Structure: gray and white matter; lots of ridges; divided by a central fissure into two lobes (R and L) connected by the vermis
Function:
- reflexive, involuntary fine-tuning motor control
- maintaining balance and posture (via connections with medulla and midbrain)
Pons
Structure and Function
Structure: between the midbrain and medulla
- houses the nuclei for CN V to CN VIII
Function: acts as a “bridge” to transmit information from cerebellum to brainstem & between the two cerebellar hemispheres
Medulla Oblongata
Structure and Function
aka myelencephalon
Structure: lowest portion of the brainstem
- nuclei of CN IX (9) through XII (12) also located here
Function: controls reflex activities - HR, RR, BP, coughing, sneezing, swallowing, and vomiting
- the medulla is also where a lot of descending motor pathways decussate
The term for motor nerves crossing contralaterally in the medulla oblongata is
decussate (crossing to the other side)
Spinal Cord
Structure and Function
Structure: lies within the vertebral canal, protected by vertebral column
- originates in medulla oblongata, ends at L1 or L2 in adults
Function:
- connects brain and body
- conducts somatic and autonomic reflexes
- provides motor pattern control centers
- modulates sensory and motor function
The cone shaped structure at the end of the spinal cord is termed
conus medullaris
At the end of the spinal cord, spinal nerves continue downwards and form a nerve bundle known as
cauda equina (like a horse’s tail)
What filament anchors the conus medullaris to the coccyx?
filum terminale
The ____________ lies in the center of the butterfly-shaped gray matter in a cross section of a spinal cord. It originates from the __________, extends through the spinal cord and is filled with _________.
central canal; fourth ventricle; CSF
The gray matter of the spinal cord is divided into three regions, which are what?
Describe their composition.
1) Posterior horn/dorsal horn: primarily interneurons and sensory neuron axons (cell bodies in dorsal root ganglion)
- substantia gelatinosa: a structure located at the tip of the posterior horn that is involved in pain transmission
2) Lateral Horn: contains cell bodies involved with ANS
3) Anterior horn/ventral horn: contains cell bodies for efferent pathways that leave the spinal cord via spinal nerves
Spinal tracts exist in (gray/white) matter. How are they named?
white matter
named based on where they begin and end (ex. spinothalamic tract = carries nerve impulses from spinal cord to thalamus)
Spinal tracts are grouped into _______ according to their location within the white matter. These groups include:
Columns
anterior, lateral and posterior (dorsal) columns
What are reflex arcs?
neural circuits in the spinal cord that control a reflex; responds to stimuli as a protective mechanism
Components:
- receptor
- afferent (sensory neuron)
- efferent (motor neuron)
- effector muscle/gland
motor effects of reflex arcs generally occur before the event (ex. touching a hot stove) is even registered and perceived in higher centers of the brain (i.e. you even realizing you’re touching a hot stove, you’ve already pulled away)
Upper motor neurons (UMNs) vs Lower motor neurons (LMNs)
Location/Structure and Function
Upper motor neurons (UMNs): completely contained within CNS
- primary role: controlling fine motor movement and influencing/modifying spinal reflex arcs and circuits
- synapse with interneurons
Lower motor neurons (LMNs): cell bodies originate gray matter of brainstem and spinal cord & projections out of CNS into PNS
- directly influence muscles
- interneurons synapse with LMNs
Composition of a motor unit
neuron and the skeletal muscle it stimualtes
The region between the axon of a motor neuron and plasma membrane of a muscle call is called the __________________.
Neuromuscular (myoneural) junction (NMJ)
List the 5 clinically relevant motor pathways
In the pyramidal system:
- corticospinal tract
- corticobulbar tract
Extrapyramidal system:
- reticulospinal tract
- vestibulospinal tract
- rubrospinal tract
Reticulospinal tract
Structure and Function
Struction: arises in the reticular formation of medulla or pons; termins within spinal cord
Function: controls body movements by inhibiting and exciting spinal activity; for balance and posture
Vestibulospinal tract
Structure and Function
Structure: origins from vestibular nucleus in the pons
Functions: causes extensor muscles of the body to rapidly contract (such as seen when someone starts to fall backwards); in charge of maintaining balance while a person is preparing for movement
Rubrospinal tract
Structure and Function
Structure: originates in red nucleus, decussates and terminates in the cervical spinal cord
Function: involved with muscle movement and fine muscle control in UE
What are the three important spinal afferent sensory pathways?
posterior column
anterior spinothalamic tract
lateral spinothalamic tract
Posterior (dorsal) column
Structure and Function
Structure: 3-neuron chain
- 1st neuron: sensory neuron (afferent) - synapses at medulla oblongtata
- 2nd neuron: crosses contralaterally at medial lemniscus and synapses in thalamus
- 3rd neuron: originates in thalamus, continues into cerebral cortex
- forms two large bundles of nerve fibers: fasciculus gracilis and fasciculus cuneatus
Function: carries fine-touch sensation, two-point discrimination, and propioceptive/epicritic information
Anterior spinothalamic tract
Structure and Function
Structure: 3-neuron chain
- primary afferent neuron (1st neuron): synapses in posterior horn of spinal cord
- 2nd order neuron: crosses contralaterally in the lateral column and ascends to thalamus
- 3rd neuron: thalamus to cerebral cortex
Function: vague touch sensation (protopathic)
Lateral Spinothalamic tract
Structure: same as anterior spinothalamic tract - 3-neuron chain
- primary afferent neuron (1st neuron): synapses in posterior horn of spinal cord
- 2nd order neuron: crosses contralaterally in the lateral column and ascends to thalamus
- 3rd neuron: thalamus to cerebral cortex
Function: pain and temp perception (protopathic)
The cranium is composed of ____ bones
8
Galea aponeurotica - what is it?
thick fibrous band of tissue that lies over the cranium between frontal and occipital muscles as added protection to the skull
How is the cranial floor divided and what brain structures lie in each respective division?
divided into three fossae (depressions)
anterior fossa: front lobes
middle fossa: temporal lobes, base of diencephalon
posterior fossa: cerebellum
Describe the layers of the meninges.
Dura mater: composed of two layers with venous sinuses between them
- outer layer: periosteum (endosteal layer)
- inner layer: inner dura (meningeal layer) - forms rigid membranes that support and separate brain structures
Arachnoid mater: spongy, web-like structure that follows the conoturs of cerebral structures
Pia mater: delicate layer that adheres to contours of the brain and spinal cord; supports blood vessels serving brain tissue
Meninges covers the brain and continues done the spinal cord, continue beyond the end of the spinal cord to the sacrum
Falx Cerebri
Structure and Function
Structure: a fold of the dura mater that dips between the two cerebral hemisphers along the longitudinal fissure
- anchored to the ethmoid bone
Function: separates the two cerebral hemispheres
Tentorium cerebelli
fold/membrane of the dura mater that seprates cerebellum and cerebrum
Subdural space
space between dura and arachnoid mater that contains lots of little bridging veins
The structures that arise from the pial membrane and produce CSF are known as _________________.
choroid plexuses
True or false. The meninges forms potential AND real spaces.
True
Epidural space
aka extradural space
a potential space between dura mater and skull
Describe what cerebrospinal fluid (CSF) is, what produces it, and what is the purpose/function of CSF.
a clear, colour fluid (similar to blood plasma and IF) that allows intracranial and spinal cord structures to float in and prevent tugging of structures/vessels/roots, therefore serves as protection
produced by choroid plexuses in the lateral, third, and fourth ventricles (a highly-vascularised structure of epithelial cells located in the ventricles of the brain)
How much CSF is circulating wtihin the ventricles and subarachnoid space at any given time?
How much CSF is produced daily?
125-150ml (circulating at any given time)
600ml produced daily
What causes CSF to flow through the CNS?
- CSF flow results from pressure gradient between arterial system and CSF-filled cavities
- CSF exerts ~5 - 14 mmHg (or 80-180mm of water pressure) on brain and spinal cord when supine, doubles when patient is upright
Describe the pathway in which CSF flows through
1) CSF formed from the blood and secreted via choroid plexuses
2) begins in lateral ventricles and flows through interventricular foramen (foramen of Monro) into third ventricles
3) then passes through cerebral aqueduct (aqueduct of Sylvius) into fourth ventricle
4) Fourth ventricle to then passing through paired lateral apertures (foramen of Luschka) or median aperture (foramen of Magendie) to subarachnoid spaces
5) reabsorbed into venous circulation through arachnoid villi
Function of arachnoid villi
reabsorbs CSF and functions as one-way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space
Vertebral column divisions
7 cervicle
12 thoracic
5 lumbar
5 fused sacral
4 fused coccygeal
Between each vertebrae (except fused sacral and coccygeal vertebrae) is an _________________
intervertebral disk
Intervetebral disk
Structure and Function
Structure: in between each vertebrae; at the center has a pulpy mass of elastic fibers (nucleus pulposus)
Function: absorbs shocks, prevent damage to vertebrae
Why are intervertebral disks one of the most common sources of back problems?
because where there is too much stress applied to the vertebral column, the disk contents may rupture and protrude into the spinal canal, which then causes compression of the spinal cord or nerve roots
What is the primary regulator for blood flow within the CNS?
CO2 - a potent vasodilator and ensures an adequate blood supply
i.e. hypoxia with increased CO2 levels would cause vasodilation to increase blood flow to the brain
What are the two systems in which the brain receives its arterial supply from?
1) Internal carotid arteries: supply greater blood flow to brain
- origin: common carotid arteries → enter cranium at base of skull → through cavernous sinus → branch and divide into anterior & middle cerebral arteries
2) Vertebral arteries: origin: subclavian arteries → through transverse foramina/foramen in cervical vertebrae → enter cranium via foramen magnum → join at junction of pons and medulla to form basilar artery → divides at level of midbrain to make posterior cerebral arteries
What is the circle of Willis?
a blood vessel system that provides an alternative route for blood flow in the event that one of the contributing arteries is obstructed (collateral blood flow)
Consists of:
- posterior cerebral arteries
- posterior communicating arteries
- internal carotid arteries
- anterior cerebral arteries
- anterior communicating artery
Describe the two classifications of cerebral veins and what structures they drain into
- classified as superficial and deep veins
- veins drain into venous plexuses and dural sinuses (between dura layers) and eventually join internal jugular veins at base of skull
Describe why it is so important for a patient with a head injury not to turn their head (besides preventing further damage to spine).
because those with head injuries who turn or let their heads fall to the side partially occlude venous return, and causing ↑ICP due to decrease flow through jugular veins
What is the blood brain barrier (BBB)? Describe its make up.
cellular structures that selectively inhibit certain potentially harmful substances in the blood from entering the interstitial spaces of the brain or CSF, which allows neurons to function normally
Composition:
- endothelial cells in brain capillaries with tight junctions
- supporting cells - astrocytes, pericytes, microglia
Describe the significance of the BBB in relation to drug therapy.
certain types of antibiotics and chemotherapeutic drugs show a greater propensity than others for crossing this barrier so understanding the mechanism of which metabolites, electrolytes, etc. may pass through compared to others
What supplies blood to the spinal cord?
from branches off the vertebral arteries & from branches from various regions of the aorta
Vertebral artery branches:
- anterior spinal artery
- posterior spinal arteries (pair)
- both^ branch at base of cranium and descend alongside spinal cord
Arterial branches:
- branches follow the spinal nerve through the intervertebral foramina, pass through the dura, and divide into the anterior and posterior radicular arteries
- radicular arteries eventually connect to spinal arteries - penetrate spinal cord to supply blood
blood return: venous draining into venous sinuses located between dura and periosteum of vertebrae
Fascicles
bundles of individual nerve fibers (myelinated axons) in the PNS
Describe the spinal nerve divisions and where they exit in the vertebrae
31 pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral pair of spinal nerves, and 1 coccygeal) - names derived from vertebral level from which they exit
first cervical nerve exist ABOVE first cervical vertebra
all the other spinal nerves exist BELOW their corresponding vertebrae
Spinal nerves contain both sensory and motor neurons and therefore are called _____________.
mixed nerves
Origin and pathway of spinal nerves
Origin: rootlets lateral to anterior and posterior horns of spinal cord
Pathway: after arising from rootlets, the two spinal nerve roots converge at the intervertebral foramen to form spinal nerve trunk → then divides into anterior and posterior rami (branches) → anterior rami form plexuses which then branch into peripheral nerves
Brachial plexus - composition and innervation
spinal nerve plexus formed by the last four cervical nerves (C5 to C8) and T1
innervates the nerves of the arm, wrist, and hand
Lumbar plexus - composition and innervation
Composition: L1 to L4 spinal nerves
Innervation: anterior portions of lower body
Sacral plexus - composition and innervation
Composition: L5 to S5
Innervation: posterior portions of the lower body
Dermatome
area of skin that is mainly supplied by a single spinal nerve
How many pairs of cranial nerves are there and where to they originate from?
12 pairs
sensory, motor, or mixed
connected to nuclei in the brain and brainstem
List the 12 cranial nerves and whether they have sensory, motor, or both functions.
CN I: Olfactory - sensory
CN II: Optic - sensory
CN III: Oculomotor - motor
CN IV: Trochlear - motor
CN V: Trigeminal - both
CN VI: Abducens - motor
CN VII: Facial - both
CN VIII: Vestibulocochlear - sensory
CN IX: Glossopharyngeal - both
CN X: Vagus - both
CN XI: Spinal accesory - both(?) (as per textbook, although typically this is motor)
CN XII: Hypoglossal - motor
Easy way to remember:
Cranial nerves: Ooh, Ooh, Ooh To Touch And Feel Very Good Velvet. Such Heaven!
Function: Some Say Marry Money But My Brother Says Big Brains Matter More
CN I
Origin/pathway
Function
How it’s tested
Name: Olfactory
Origin and Course: arise from nasal olfactory epithelium and form synapses with olfactory bulbs, which transmit impulses to the temporal lobe
Function: sensory - carries impulses for sense of smell
How to Test: sniffing various aromatics & trying to identify them
CN II
Origin/pathway
Function
How it’s tested
Name: Optic
Origin & Course: arise from eye retina to form optic nerve & through sphenoid bone; two optic nerves converge to form optic chiasma (with partial crossover of fibers) and eventual to occiptal cortex
Function: sensory - carries impulses for vision
How it’s Tested: vision & visual field tested via eye chart and testing when a person sees a finger moving into their visual field
- eye interior is viewed with ophthalmoscope to look at blood vessels
CN III
Origin/pathway
Function
How it’s tested
Name: Oculomotor
Origin & Course: emerge from midbrain and exit from skull, runs to eye
Function: mainly motor - eye muscle function and pupil response
- goes to inferior oblique & superior, inferior, and medial rectus extraocular muscles that direct eyeball
- levator muscles of eyelid
- smooth muscles of iris & ciliary body
- DOES support sensory functioning (proprioception) to brain from extraocular muscles
How it’s tested: examine pupils (size, shape, equality); penlight to test reactivity; ability to follow moving object
CN IV
Name
Origin/pathway
Function
How it’s tested
Name: Trochlear
Origin and Course: emerge from posterior midbrain and exist from skull to run to eye
Function: motor - innervate superior obliqud muscle of eye (extraocular muscle)
How it’s Tested: tested with CN III relative to ability to follow moving objects
CN V
Name
Origin/pathway
Function
How it’s tested
Name: Trigeminal
Origin and Course: emerge from pons and form three divisions that exit from skull, run to face and cranial dura mater
Function: motor and sensory for face
- conducts sensory impulses from mouth, nose, eye surface, and dura mater
- motor fibers that stimulate chewing muscles
How it’s tested:
- senation for pain, touch and temp: safety pin and hot/cold objects
- corneal reflex tested with wisp of cotton
- motor branch tested by asking pt to clench teeth, open mouth against resistance, move jaw from side to side
CN VI
Name
Origin/pathway
Function
How it’s tested
Name: Abducens
Origin and Course: fibers leave inferior pons and exit from skull to run to eye
Function: motor - fibers to lateral rectus muscle, and proprioceptor fibers from same muscle to brain
How it’s tested: along with CN III relative to ability to move each eye laterally
CN VII
Name
Origin and Course
Function
How it’s tested
Name: Facial
Origin and Course: leave pons and travel through temporal bone to reach face
Function: sensory and motor
- Motor: muscles for facial expression & to lacrimal and salivary glands
- Sensory: taste buds of anterior part of tongue
How it’s tested:
- anterior 2/3rds of tongue tested for sweet, salty, sour, bitter
- face symmetry checked
- subject asked to close eyes, smile, whistle, etc.
- tearing tested with ammonia fumes
CN VIII
Name
Origin and Course
Function
How it’s tested
Name: Vestibulococchlear
Origin and Course: run from inner eat (hearing and equilibrium receptors in temporal bone) to enter brainstem just below pons
Function: sensory - sense of equilibrium & hearing
How it’s tested: hearing checked by tuning fork; vestibular tests: Bárány and caloric tests
CN IX
Name
Origin and Course
Function
How it’s tested
Name: Glossopharyngeal
Origin and Course: emerge from medulla and leave skull to run to throat
Function: sensory and motor
- motor: serves pharynx (throat) and salivary glands
- sensory: carry impulses from pharynx, posterior tongue (taste buds), and pressure receptors of carotid artery
How it’s tested:
- gag and swallow reflex
- asked to speak and cough
- posterior 1/3rd of tongue tested for taste
CN X
Name
Origin and Course
Function
How it’s tested
Name: Vagus
Origin and Course: emerge from medulla, pass through skull, & descend through neck region into thorax and abdo region
Function: sensory and motor
- carry sensory and motor impulses for pharynx
- parasympathetic motor fibers which supply smooth muscles of abdo organs
- receives sensory impulses from viscera
How it’s tested: same as CN IX (checking gag and swallow reflex; speaking, coughing, taste)
CN XI
Name
Origin and Course
Function
How it’s tested
Name: Spinal accessory
Origin and Course: arise from medulla and superior spinal cord and travel to muscles of neck and back
Function: sensory and motor fibers for sternocleidomastoid and trapezius muscles and muscles of soft palate, pharynx, and larynx
How it’s tested: sternocleidomastoid and trap muscles checked for strength - rotate head and shrug shoulders against resistance
CN XII
Name
Origin and Course
Function
How it’s tested
Name: hypoglossal
Origin and Course: fibers arise from medulla and exit from skull to travel to tongue
Function: carries motor fibers to muscles of tongue and sensory impulses from tongue to brain
How it’s tested: stick out tongue to note position abnormalities if any
What does the motor component of the ANS consist of?
two neuron system
preganglionic neurons (myelinated) - conduct impulses from brainstem or spinal cord to an autonomic ganglion where they synapse with postganglionic neuron
postganglionic neurons (unmyelinated) - conduct impulses away from ganglion to the effector
Function of the ANS
coordinates and maintains a steady state among visceral (internal) organs (ie regulation of cardiac muscle, smooth muscle, and glands); an involuntary system
Describe how the axons in the sympathetic nervous system are set up.
- innervated by cell bodies located in the thoracolumbar division (T1 to L2 of spinal cord)
- preganglion axons form synapses SHORTLY after leaving spinal cord in the sympathetic (paravertebral) ganglia; then travels in one of the following ways
- 1) directly synapses with postganglionic neurons in sympathetic chain ganglion at their level
- 2) traveling up or down sympathetic chain ganglion before synapsing with higher/lower postganglionic neuron
- 3) through the sympathetic chain ganglion to synapse with collateral ganglia
What are splanchnic nerves and collateral ganglia?
splanchnic nerves are pathways formed by a group fo preganglionic axons that eventually innervate the abdomen
splanchnic nerves lead to collateral ganglia (which lies in front of the aorta) and branch into celiac, superior mesenteric, & inferior mesenteric ganglia which then eventually postganglionic neurons leave and innervate viscera
Describe how the axons in the parasympathetic nervous system are set up.
- nerve cell bodies are located in the craniosacral division (cranial and sacral regions of the spinal cord)
- from cranial: CN III (oculomotor), VII (facial), IX (glossopharyngeal), and X (vagus)
- from sacral: form pelvic splanchnic nerve that innervates pelvic cavity viscera
- preganglgionic fibers travel close to the organs they supply before synapsing (so they have short postganglionic neurons)
Sympathetic preganglionic & parasympathetic pre- and post-ganglionic fibers what neurotransmitter? This is known as ________ transmission.
Acetylcholine; cholinergic transmission
Most postganglionic sympathetic fibers release what neurotransmitter? This is considered __________ transmission.
Norepineprhine; adrenergic transmission
*some post-ganglionic sympathetic fiebrs release ACh (like those that innervate sweat glands but MOST release norepi)
The two types of adrenergic receptors are what? Describe their subdivisions and general function.
𝜶 and 𝜷
𝜶1 receptors: excitation or stimulation
𝜶2 receptors: relaxation or inhibition
𝜷1 receptors: faciliated increased HR and contractility, cause release of renin from kidney
𝜷2 receptors: stimulates smooth muscle relaxation
Describe which adrenergic receptors are stimulated by norepinephrine and epinephrine.
Norepinephrine: ALL 𝞪1 and 𝞫1 receptors and only certain 𝞫2 receptors
- primary response is stimulation of 𝞪1 receptors causing vasoconstriction
Epinephrine: strongly stimulates all four types of receptors and induces general vasodilation (on beta receptors) due to the predominance of 𝞫 receptors in muscle vasculature
Functions of the ANS
- fight of flight response
- rest and tranquility response
- opposing effects between sympathetic and parasympathetic divisions to maintain a steady state in the internal environment
Structural changes to the neurological system with aging
- decreased brain weight and size (particularly frontal regions)
- increased in ventricular volume & size
- fibrosis and thickening of meninges
- narrowing of gyri and widening of sulci
Cellular changes to the neurological system with aging.
- decreased # of neurons, dendritic processes, and synaptic connections
- decreased myelin
- lipofuscin deposition (a pigment resulting from cellular autodigestion)
- neurofibrillary tangles (++ accumulation in cortex associated with Alzheimers)
- imablance in amoutn and distribution of NTs
- decrease in glucose metabolism
Cerebrovascular changes with aging
- arterial atheroscelrosis (leading to risk of infarcts and scars)
- increased permeability of BBB
- decreased vascular density
Functional changes with aging secondary to neurological changes.
varies from individual to individual
- decreased tendon reflexes
- progressive deficit in taste and smell
- decreased vibratory sense
- decrease in accommodation and colour vision
- decrease in neuromuscular control with change in gait and posture
- sleep disturbances
- memory impairments & cognitive alterations
Define pain
unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
a protective phenomenon, unique to the individual (i.e. cannot be defined, identified, or measured by an observer)
Why is acute pain considered “protective”?
because it promotes withdrawing from painful stimuli, which allows the injured part to heal and makes us learn to avoid painful stimuli
What are the three portions of the nervous system responsible for sensation, perception and response to pain?
1) Afferent pathways: start in the PNS, travel through spinal cord and then up to higher centers in CNS
2) Interpretive centers: in brainstem, midbrain, diencephalon, and cerebral cortex
3) Efferent pathways: descend from CNS back to dorsal horn of spinal cord
The processing of potentially noxious stimuli through a normally functioning nervous system is known as
nociception
What are nociceptors? Also describe their composition and what types of stimuli they respond to.
- pain receptors - free nerve endings in the afferent PNS that cause nociceptive pain when stimulated
- cell bodies located in dorsal root ganglia (DRG) for the body & in trigeminal ganglion for the face
- unevenly distributed throughout body so pain sensitivity differs
- responds to different types of noxious stimuli
- mechanical (pressure, mechanical distortion)
- thermal (extreme temps)
- chemicals (acids, inflammatory chemicals - bradykinin, histamine, leukotrienes, prostaglandins)
What are the four phases of nociception?
1) Pain transduction
2) Pain transmission
3) Pain perception
4) Pain modulation
Describe the 1st phase of nociception: pain transduction
- begins when nociceptors are axtivated by noxious stimulus
- Na, K, and Ca ion channels on receptors open to create electrical impulses that travel through the 2 primary types of nociceptor axons
- A-delta fibers
- C fibers
Describe the two primary types of nociceptors
A-delta (A𝜹) fibers: large myelinated fibers, rapidly transmit sharp & well-localized “fast” pain sensations (like burns or pinpricks to the skin)
- when activated, causes spinal reflex withdrawal of body part BEFORE a pain sensation is perceived
C fibers: most numerous, smaller & unmyelinated; located in muscle, tendons, body organs, skin
- slowly transmit dull, aching, or burning sensations that are poorly localized and often constant
Describe the 2nd phase of nociception: Pain transmission (including its pathways)
- the conduction of pain impulses along the A𝛿 and C fibers (primary order neurons) into dorsal horn of spinal cord
- neurons synapse with excitatory or inhibitory interneurons (second order neurons) in substantia gelatinosa of dorsal horn
- impulses then synapse with projection neurons (third order neurons), cross midline of spinal cord, and ascend brain through lateral spinothalamic tracts
- anterior spinothalamic tract: carries fast impulses for acute sharp pain (perceived first)
- lateral spinothalamic tract: carries slow impulses for dull/chronic pain
- impulses then projected into different structures of the brain then to sensory areas for interpretation
Describe the 3rd phase of nociception: pain perception
- the conscious awareness of pain (influenced by genetics x environment)
- occurs primarily in reticular and limbic systems and cerebral cortex
- three systems interacting to produce perception: aka the “pain matrix”
- sensory-discriminative: mediated by somatosensory cortex; identifying presence, character, location, and intensity of pain
- affective-motivational: mediated by reitcular formation, limbic system, and brainstem; determines someone’s conditioned avoidance behaviours & emotional response to pain
- cognitive-evaluative: mediated through cerebral cortex; oversees learned behaviours from previous experiences and modulate perception of pain
Pain threshold vs pain tolerance
Pain threshold: defined as lowest intensity of pain that a person can recognize (i.e. lowest point at which a stimulus is perceived as pain)
- intense pain in one location can increase pain threshold in another location (like distracting painful injuries; known as perceptual dominance); threshold can also be raised by various factors like exercise, sex, stress, etc.
Pain tolerance: defined as the greatest intensity of pain that a person can handle; varies between people and in the same person overtime
- may decrease with: repeated exposures to pain, fatigue, anger, boredom, apprehension, & sleep deprivation
- increase with: alcohol consumptino, persistent opioid med use, hypnosis, distraction, strong beliefs/faith
Describe the 4th phase of nociception: pain modulation
- facilitation or inhibition of transmission of pain signals throughout nervous system; can occur before, during, or after pain perception
- done through NTs
-
Excitatory NTs: triggered by tissue injury and/or inflammation - glutamate, aspartate, substance P, calcitonin
- reduces activation threshold so increased responsiveness from nociceptors
- Inhibitory NTs: GABA, glycine; serotonin and norepinephrine inhibit pain in the medulla and pons
-
Excitatory NTs: triggered by tissue injury and/or inflammation - glutamate, aspartate, substance P, calcitonin
What are endogenous opioids and what is their function?
What are they? A family of morphine-like neuropeptides that inhibit pain transmission in the periphery, spinal cord, and brain
How they work: binds to specific opioid receptors (mu, kappa, delta) on neurons which inhibits ion channels and thus release of excitatory NTs
Location and function of opioid receptors
found widely distributed throughout body
responsible for general sensations of well-being and modulation of many physiological processes (controlling resp and CV functions, stress and immune responses, GI function, reproduction, and neuroendocrine control)
Types of endogenous opioids
- Enkaphalins - most prevalent of the natural opioids, binds to 𝛿 opioid receptors
- Endorphins - endogenous morphine produced in the brain (sense of exhilaration and natural pain relief)
- Dynorphins - most potent, binds to kappa receptors to impede pain signals
- Endomorphins - bind with mu receptors, analgesic effects
- Nocicpetin/orphanin FQ - induces pain or hyperalgesia but does not interact with opioid receptors
bind as direct agonists to opioid receptors
The only clinically used opioid receptor antagonist is __________ and has a higher affinity for which opioid receptors?
naloxone; mu receptors
What are endocannabinoids?
- substances in our bodies synthesized from phospholipids that activate CB1 (primarily in CNS) and CB2 (primarily in immune tissue) receptors to modulate pain
- classified as eicosanoids
- CB1 receptors decrease pain transmission by inhibiting release of excitatory NTs in various structures within brain and spinal cord
How does cannabis provide an analgesic effect?
cannabis produces a resin that contains cannabinoids, which are analgesic in humans (drawbacks: psychoactive and addictive properties)
Describe how the descending inhibitory and facilitatory pain pathways modulate pain
- inhibitory pathways activate opioid receptors and inhibit release of excitatory NTs, facilitate release of inhibitory NTs, and stimulate inhibitory interneurons
- afferent stimulation of ventromedial medulla and periaqeductal gray (PAG) in midbrain stimulates efferent pathways which inhibit ascending pain signals
How does segmental pain inhibition modulate pain?
- occurs when A-beta (A𝞫) fibers are stimulated and inhibitory interneurons and decrease pain transmission
- ex. rubbing an area that has been injured to relieve pain
How does the diffuse noxious inhibitory control (DNIC) system modulate pain?
- aka heterosegmental pain inhibition
- inhibits pain when two noxious stimuli occur at the same time from different sites (pain inhibiting pain)
- used clinically in pain relief techniques - acupuncture, deep massage, intense cold/heat
How does expectancy-related cortical activation (i.e. placebo effect and nocibo effect) modulate pain?
Placebo effect: when an inert substance provokes perceived benefits
Nocibo effect: when an inert substance provokes perceived harm
expectations can exert control over analgesic systems to attenuate/intensify pain (i.e. cognitive expectations can cause measurable physiological effects)
What is acute pain?
- a normal protective mechanism (to alert that something is immediately harmful to the body and mobilizes the person to take action to relieve it)
- transient, usually lasting seconds to days or up to 3 months
- begins suddenly and is relieved after the removal of pain stimulus
What are the three classifications of acute pain?
1) Somatic pain: arises from skin, joints, & muscles
- if carried by A𝛿 fibers: sharp and localized
- if carried by C fibers: dull, aching, throbbing
2) Visceral pain: refers to pain in internal organs and body cavity linings
- transmitted by C fibers and tends to be poorly located with aching, gnawing, throbbing, or intermittent cramping quality
- carried by sympathetic fibers & associated with N/V, hypotension, and sometimes shock
- often radiates or is referred
3) Referred pain: pain that is felt in an area distant from its point of origin - due tot he area of referred pain being supplied by the same spinal segment as the actual site of pain
- can be acute/chronic
What is chronic/persistent pain?
- pain lasting for more than 3-6 months and is pain lasting well beyond the expected normal healing time
- serves no purpose
- often out of proportion to any observable tissue injury
- can be ongoing or intermittent; sudden or insidious onset
- thought to be due to dysregulation of nociception and pain modulation processes
- produces significant behavioural and psychological responses:
- decreased ability to cope
- stress, depression, eating and sleeping difficulties
What is neuropathic pain?
- chronic pain initiated/caused by primary lesion or dysfunction in the nervous system, leading to long term changes in pain pathway structures (neuroplasticity) and abnormal processing of sensory information
- pain is amplified without stimulation of injury or inflammation
- burning, shooting, shocklike, or tingling sensation
- these patients have increased sensitivity to painful or nonpainful stimuli (hyperalgesia, allodynia, or spontaneous pain)
Allodynia
condition where pain is induced by normally nonpainful stimuli
What are the two classifications of neuropathic pain?
1) Peripheral neuropathic pain: caused by peripheral nerve lesions & increased sensitivity and excitability of primary sensory neurons and cells in DRG (peripheral sensitization)
- ex. nerve entrapment, diabetic neuropathy, chronic pancreatitis
2) Central neuropathic pain: caused by a lesion or dysfunction in the brain/spinal cord
- group C neurons in the dorsal horn are progressively stimulated leading to icnreased sensitivity of central pain signaling neurons (central sensitization) leading to chronic pain
- ex. brain or CBI, tumors, MS, parkinson’s phantom limb pain
Body temperature in both genders tend to peak when? When are they the lowest?
peak: ~6PM
lowest: during sleep
Body temperature varies in response to all the following except:
a) location
b) height
c) activity
d) environment
e) circadian rhythm
f) gender
b) height
Thermoregulation is regulated by what two main systems?
Through what receptors do these two systems use to thermoregulate?
- mediated by hypothalamus and endocrine system
- hypothalamus gets its informtion from:
- peripheral thermoreceptors (in skin and abdo organs) - C and Aδ fibers
- central thermoreceptors (in hypothalamus, spinal cord, abdo organs, etc.)
- triggers heat production and heat conservation or heat loss mechanisms
How is body heat produced?
1) chemical reactions of metabolism (aka nonshivering thermogenesis)
- thryotropin releasing hormone (TRH) from hypothalamus stimulates anterior pituitary to release TSH
- TSH acts on thyroid, thyroxine released
- thyroxine acts on adrenal medulla, epinephrine is released
- epinephrine causes cutaneous vasoconstriction, stimulates glycolysis, and increased metabolic rate to generate body heat
- norepinephrine and thyroxine also activate brown fat thermogenesis where energy is released as heat
2) skeletal muscle tone and contraction - shivering & vasoconstriction to conserve heat
- hypothalamus triggers SNS which stimulates adrenal cortex to increase skeletal muscle tone
- peripheral blood vessels are constricted to shunt blood away and to the core for heat retainment
3) Relay information to higher centers - hypothalamus relays information to cerebral cortex of cold leading to people bundling up, keeping active, or curl up in a ball
How does the hypothalamus respond to warmer core and peripheral temperatures?
- reversing same mechanisms as heat conservation
- heat loss done through:
- radiation
- conduction
- convection
- vasodilation
- evaporation (sweating)
- decreased muscle tone
- increased respiration
- voluntary mechanisms (like taking off clothes)
- adaptations to warmer climates (i.e. how much sweating occurs)
Why do infants struggle with maintenance of their body temperature?
- infants produce sufficient body heat (primarily through metabolism of brown fat) HOWEVER cannot conserve heat due to:
- small body size
- greater body surface to body weight ratio
- inability to shiver
- less subQ fat so not as well insulated as adults
Why do the elderly struggle with maintenance of their body temperature?
- slowed blood circulation
- structural and functional skin changes
- overall decreased heat producing activities (decreased shivering response)
- presence of disease (like CHF, DM, etc.)
- slowed metabolic rate
- decreased vasoconstrictor response
- diminished ability to sweat
- decreased peripheral sensation
- desynchronized circadian rhythm
- decreased perception of heat and cold
- decreased brown adipose tissue
What is a fever?
a temporary resetting of the hypothalamic thermostat to a higher level in response to exogenous or endogenous pyrogens
How do exogenous and endogenous pyrogens cause fever?
- exogenous pyrogens stimulate the release of endogenous pyrogens from phagocytic cells
- pyrogens then raise the thermal set point by inducing prostaglandin E2 (PGE2) synthesis by the hypothalamus
- body temperature is thus raised via heat production and conservation
What happens once the internal temp is set at a new and higher set point during fever?
The pt feels colder so they dress warmly, curl up, etc. to stay warm
body temp is maintained at that new level until the fever “breaks” meaning the set point begins to return to normal with decreased heat production and increased heat reduction mechanisms
Fever of unknown origin (FUO)
a body temp of > 38.3°C (101°F) for longer than 3 weeks’ duration that remains undiagnosed after 3 days of hospital investigation, 3 outpatient visits, or 1 week of ambulatory investigation
What are the benefits to a fever?
- Higher body temp kills many microorganisms and adversely affects their growth and replication
- Decreases serum levels of iron, zinc, and cooper - minerals needed for bacterial replication
- Causes lysosomal breakdown and autodestruction of cells, preventing viral replication in infected cells
- heat increases lymphocytic transformation and motility of polymorphonuclear neutrophils, facilitating the immune response
- enhanced phagocytosis & production of antiviral interferon (to block virus replication)
How do the effects of fever present in children and elderly?
Children:
- they develop higher temps than adults for relatively minor infections
- febrile seizures before 5 are not uncommon
Elderly:
- show decreased or no response to infection (therefore benefits of fever are reduced)
- high morbidity and mortality result from lack of benefits from fever
Describe what hyperthermia is and its potential effects.
- elevation of the body temp without and increase in the hypothalamic set point
- At 41°C (105.8°F) - nerve damage leading to convulsions
- At 43°C (109.4°F) - death
- also cause coagulation of cell proteins
- can be therapeutic, accidental, or associated with stroke or head trauma
Therapeutic vs accidental hyperthermia
Therapeutic hyperthermia: method used to destroy pathologic microorganisms/tumor cells by facilitating host’s natural immune process or tumor blood flow; can be localized or systemic
Accidental hyperthemia: heat cramps, heat exhaustion, and heat stroke; also malignant hyperthemia
What are heat cramps?
- severe, spasmodic cramps in abdomen and extremities that happen after prolonged periods of sweating and sodium loss
- usually in those that are not accustomed to heat or doing strenuous work in very warm climates
- S/S: cramping, fever, high HR & BP
What is heat exhaustion?
- condition resulting from polonged high core or environmental temps
- causes profound vasodilation and profuse sweating which leads to dehydration, decreased plasma volumes, hypotension, decreased cardiac output, and tachycardia
- S/S: weakness, dizziness, confusion, nausea, fainting
What is heat stroke? Describe potential causes, signs/symptoms, as well as complications.
- potentially lethal result of an overstressed thermoregulatory center
- Causes: exertion, overexposure to environmental heat, impaired physiological mechanisms for heat loss
- core temp is >40°C (104°F) causing regulatory center to stop functioning and thus heat loss mechanisms
- S/S: high core temp, no sweating, rapid HR, confusion, agitation, coma
- Complications: cerebral edema (any fluid left in body is pushed to the brain to keep it functioning), CNS degeneration, swollen dendrites, renal tubular necrosis, hepatic failure with delirium, coma, eventually death if no tx
What is malignant hyperthermia? Describe what it is, the pathophysiology, and clinical manifestations
Definition: hypermetabolic complication of a rare inherited muscle disorder, triggered by inhaled anesthetics and depolarizing muscle relaxants; most common in chidlren and adolescents
Pathophysiology: involves altered calcium function in muscle cells with:
- hypermetabolism
- uncoordinated muscle contractions
- increased muscle work & O2 consumption
- raised level of lactic acid production
Manifestions: acidosis & increased body temp leading to increased HR, cardiac dysrhythmias, hypotension, decreased cardiac output, cardiac arrest
- coma-like (unconscious, absent reflexes, fixed pupils, apnea, flat ECG
- oliguria/anuria common
Describe what hypothermia is and its potential effects on the body.
What it is: core body temp <35°C (95°F)
Effects: depresses CNS and resp system, cause vasoconstriction, alterations in microcirculation and coagulation, and ischemic tissue damage
- in severe hypothermia, ice crystals form inside the cell causing them to rupture and die
- slows metabolism
- increases blood viscosity
- slow microcirculatory blood flow
- facilitates blood coagulation
Types: accidental or therapeutic
Accidental Hypothermia
Definition, Causes, Risk Factors, Phsyiological Responses, Treatment
What is it: unintentional decrease in core temp (<35°C or 95°F)
Causes: sudden immersion in cold water, prolonged exposure to cold environments, diseases that diminiah ability to generate heat, altered thermoregulatory mechanisms
Risk factors:
- common in young and elderly persons
- hypothyroidism
- hypopituitarism
- Parkinson’s
- RA
- Chronic increased vasodilation
- Failure of thermoregulatory control 2’ to cerebral injury, ketoacidosis, uremia, sepsis, or drug OD
Physiological Responses:
- Peripheral vasoconstriction - blood shunted away from cooler skin to core to reduce heat loss, produces peripheral tissue ischemia
- Intermittent reperfusion of extremities (Lewis phenomenon) - helps preserve peripheral oxygenation until core temp drops dramatically
- Shivering - induced by hypothalamus; thinking becomes sluggish, depressed coordination
- Stupor - decreased HR, RR, cardiac output, metabolic rate; acidosis, eventual VF and asystole at 30°C or lower
Treatment:
- rewarming
- active rewarming (external) for core temp >30°C
- active rewarming (internal) for core temp <30°C or those with severe CV problems
What is therapeutic hypothermia used for, and what effeccts/risks may it have?
Use: to slow metbaolism and preserve ischemic tissue during surgery (like limb reimplantation), after cardiac arrest, or following neurological injury
Effects:
- stresses the heart, leading to VF and cardiac arrest
- exhausts liver glycogen stores by prolonged shivering
- surface cooling may cause burns, frostbite, and fat necrosis
- immunosuppression with increased infection risk
How does major body trauma causes changes in body temp?
- damage to the CNS (inflammation, increased ICP, intracranial bleeding) can lead to central fever (body temp >39C)
- does not induce sweating
- very resistant to anti-pyretic therapy
- can also be caused by accidental injuries, hemorrhagic shock, major surgery, and thermal burns
What is sleep and what is it controlled by?
What it is: an active, multiphase process that provides restorative functions and promotes memory consolidation; two phases: REM and non-REM
Controlled by: neural circuits, hormones, NTs that involve the hypothalamus, thalamus, brainstem and cortex
- controls sleep-wake cycle & coordination with circadian rhythms
REM vs non-REM sleep
REM sleep: 20-25% of sleep time
non-REM sleep: slow-wave sleep; further divided into three stages (N1, N2, N3) from light to deep sleep followed by REM sleep
How many cycles of REM and non-REM sleep occur each night in the average adult?
4-6 cycles
What brain structure is the “major sleep center”?
Describe what substances are released by this sleep center that promotes wakefulness vs sleep.
Major sleep center: hypothalamus
Promotes wakefulness: hypocretins (orexins), ACh, glutamate
Promotes Sleep: Prostaglandin D2, adenosine, melatonin, serotonin, L-tryptophan, GABA and growth factors
- reticular formation primarily responsible for generating REM sleep
- projections from the thalamocortical network produce non-REM sleep
Describe how REM sleep is initiated and what happens during this time?
- initiated by REM-on an REM-off neurons in the pons and mesencephalon
- REM sleep occurs about every 90 minutes beginning one to two hours after non REM sleep begins
- known as paradoxical sleep because the EEG pattern is similar to that of the normal wake pattern and the brain is very active with dreaming.
REM and non REM sleep alternate throughout the night, with lengthening intervals of REM sleep and fewer intervals of deeper stages of non REM sleep toward the morning.
Changes:
- parasympathetic activity and variable sympathetic activity associated with rapid eye movement
- Muscle relaxation
- Loss of temperature regulation
- Altered heart rate, blood pressure, and respiration
- Penile erection in men and clitoral engorgement in women
- Release of steroids
- memorable dreams.
Respiratory control appears largely independent of metabolic requirements and oxygen variation.
Loss of voluntary muscle control in the tongue and upper pharynx may produce some respiratory obstruction.
Cerebral blood flow increases.
Describe how non-REM sleep is initiated and what happens during this time.
- 75% to 80% of sleep time in adults, initiated when inhibitory signals are released from the hypothalamus
- Sympathetic tone is decreased, and parasympathetic activity is increased during non-REM sleep, creating a state of reduced activity
- Basal metabolic rate falls by 10% to 15%
- temperature decreases 0.5° to 1° C (0.9° to 1.8° F) & heart rate, respiration, blood pressure, and muscle tone decrease
- knee jerk reflexes are absent
- Pupils are constricted
- Cerebral blood flow to the brain decreases and growth hormone is released, with corticosteroid and catecholamine levels depressed
Describe the sleep characteristics of infants
- sleep 10-16 hours daily
- 50% REM, 25% non-REM
- sleep cycles are 50-60 min in length
- At 1 year, REM and non-REM sleep cycles are about the same and infants sleep through the night + 2 daytime naps
Sleep characteristics of elderly persons (relative to healthy adults)
- total sleep time is decerease with a longer time to fall asleep and poorer quality
- total time in slow-wave and final phase of non-REM sleep decreases by 15-30%
- increases in stage 1 and 2 non-REM sleep, attributable to an increased number of spontaneous arousal
- tend to go to sleep earlier in the evening and wake earlier in the morning because of a phase advance in their normal circadian sleep cycle
- alterations in sleep patterns ~10 years later in women > men
- more likely to have sleep disorders
- increase risk of morbidity/mortality
What are the six classifications of sleep disorders?
1) insomnia
2) sleep related breathing disorders
3) central disorders of hypersomnolence
4) circadian rhythm sleep-wake disorders
5) parasomnias
6) sleep-related movement disorders
What are dyssomnias? Provide 4 examples of common dyssomnias.
Dyssomnias: sleep disorders that negatively impact quantity and quality of sleep (difficulty falling or staying asleep)
Examples:
- Insomnia
- Obstructive Sleep Apnea Syndrome (OSAS)
- Narcolepsy
- Circadian Rhythem Sleep Disorder
What is insomnia?
What it is: inability to fall or stay asleep, accompanied by fatigue during wakefulness
Characteristics:
- mild, mod, or severe
- transient (few days or months - aka primary insomnia) OR chronic
- chronic insomnia can be idiopathic, start early, associated with drug/EtOH use, chronic pain, depression, obesity, aging, genetics, or environmental factors
What are the three layers that make up the wall of the eye?
1) sclera: thick, white outermost layer & becomes transparent at the cornea (which is the portion of the sclera in the central anterior region that allows light to enter)
2) choroid: deeply pigmented middle layer that prevents light from scattering inside the eye; includes the iris which has a round opening aka the pupil where light passes through
3) retina: innermost layer of the eye; has rods and cones to convert light energy into nerve impulses
Lateral to each optic disc is the __________ the area of most distinct vision.
At the center of this structure is the ____________ which is a tiny area that contains ONLY cones and provides greatest visual acuity.
macula lutea
fovea centralis
What are the three types of refraction?
1) Myopia - nearsightedness: light rays are focused IN FRONT of the retina when someone is looking at a distant object
2) Hyperopia - farsightedness: light rays are focused BEHIND the retina when someon eis looking at a near object
3) Astigmatism - unequal curvature of the cornea: light rays are bent unevenly and do not come to a single focus on the retina; co-exist with myopia, hyperopia, or presbyopia
Injury to the R optic nerves leads to __________.
Injury to the optic chiasm leads to _____________.
Injury to the left optic tract leads to ___________.
1) Right eye blindness (usually causes same-sided blindness to the side of injury of the optic nerve)
2) Bitemporal hemianopia (visual defects/blindness in half of visual field - in this case, out visual field i.e. towards the ears)
3) Bilateral R hemianopia (visual fields on the right)
Composition of the external ear
- pinna (auricle): visible portion of the ear
- external auditory canal: tube that leads from outer to middle ear
- meatus: opening of the ear canal - just above mastoid process
Composition of the middle ear
- tympanic cavity: the cavity that surrounds the bones of the middle ear
- Three ossicles: transmits vibration of the tympanic membrane to the inner ear (from malleus to stapes)
- malleus (hammer)
- incus (anvil)
- stapes (stirrup) - presses against the oval window (small membrane of inner ear) that then sets fluids in motion in the inner ear
Composition of the inner ear
- system of osseous labyrinths (bony chambers) filled with perilymph; divided into:
- cochlea
- vestibule: eqm receptors
- semi-circular canals: eqm receptors
- a membranous labyrinth filled with endolymph is suspended in the perilymph and follows the shape of the bony labyrinth
- Organ of Corti: within cochlea; contains hair cells (hearing receptors) that transmit impulses along cochlear nerve to brain
Supratentorial disorders
- above the tentorium cerebelli
- changes arousal by diffuse or localized dysfunction
- diffuse dysfunction: caused by disease processes affecting cerebral cortex or the underlying white matter; extracerebral injuries (outside of brain but within cranium - i.e. neoplasms, closed head trauma, pus accumulation in subdural space)
- localized dysfunction: intracerebral conditions like bleeding, infarcts, emboli, tumors - these can all directly impair function of thalamic or hypothalamic activating systems
Describe what this test is.
Test for Oculocephalic Reflex Response (Doll’s Eyes Phenomenon)
A - normal response - eyes turn to the side opposite from where the head is being turned
B - Abnormal response - eyes do not turn in conjugate manner
C - Absent response - eyes move in the direction of head movement (brainstem injury)
Describe what test this is.
Test for Oculovestibular Reflex (Caloric Ice Water Test)
A - Ice water is injected into the ear canal; normal response (conjugate eye movement)
B- abnormal response - dysconjugate or asymmetric eye movements
C- absent response - no eye movements
What reflex is this?
Grasp reflex
primitive reflex – normal in the newborn but disappear in infancy. Palmar grasp reflex in adults is a pathological frontal release sign and may signify frontal lobe damage
What reflex is this?
Snout reflex
pouting or pursing of the lips induced by light tapping of the closed lips in the midline is considered a sign of frontal lobe dysfunction.
What reflex is this?
Palmomental reflex (PMR)
- a primitive reflex consisting of a twitch of the chin muscle elicited by stroking a specific part of the palm
- present in infancy and disappears as the brain matures during childhood but may reappear due to processes that disrupt the normal cortical inhibitory pathways
- Therefore, it is an example of a frontal release sign
What reflex is this?
Suck reflex
- common to all mammals and is present at birth
- Linked with rooting reflex and breastfeeding
- Causes the child to instinctively suck anything that touches the roof of their mouth, and simulates the way a child naturally eats
- This is normal in infants, but pathological in adults
Describe decorticate and decerebrate posturing
A - Decorticate posture/response: Flexion of arms, wrists and fingers with adduction in upper extremities. Extension, internal rotation and plantar flexion in lower extremities. Both sides.
B - Decerebrate posture/response: All four extremities in rigid extension, with hyperpronation of forearms and plantar extension of feet.
Alzheimer disease (AD)
Definition, Types, Pathophysiology, Clinical Manifestations, Diagnosis, Treatment
Definition: a progressive neurologic disorder that causes the brain to atrophy and brain cells to die; leading cause of severe cognitive dysfunction in elderly
Types:
- 1) nonhereditary sporadic or late onset AD (70-90%)
- 2) early onset familial AD (FAD)
- 3) early onset AD (very rare)
Pathophysiology: cause unknown but there are theories:
- mutations on chromosome 21 (abnormal amyloid precursor protein 14), abnormal presinilin 1 and 2
- alterations in apolipoprotein E (in chromosome 19)
Alterations in the brain:
- accumulation of neuritic plaques that have a core of amyloid beta protein, neurofibrillary tangles (Tau, binding protein in neuron detaches and forms insoluble filament), and degeneration of basal forebrain cholinergic neurons with loss of ACh
- amyloid protein accumulates and not processed, leading to formation of plaques, nerve impulse transmission disrupted, neuron death
- loss of neurons lead to brain atrophy, sulci widening, gyri shrinking
- loss of synapses, ACh, and other NTs lead to memory and attention decline and loss of cognitive functions
Clinical Manifestations:
- patho changes can occur decades before anything clinically appears as dementia
- Initial Sx: insidious - foregetfulness, emotionally upset, other illnesses
- progressively more forgetful esp with recent events; then becomes disoriented and confused, loses ability to concentrate
- then abstraction, problem solving, judgment gradually deteriorate, mental status, mood, and behavioural changes
- ++weight loss
- motor changes (if posterior frontal lobes affected): rigidity and flexion posturing
Diagnosis: makde by ruling out other causes (clinical hx, cognitive assessments, lab testing, brain imaging and blood flow)
Treatment: compensatory devices to help with impaired cognitive function (memory aids, improving hygiene, nutrition, and health)
Increased Intracranial pressure (IICP)
Causes & Stages of IICP
Causes: increase in intracranial content (tumor growth), edema, excess CSF, hemorrhage
- CSF most likely displaced to try and reduce volume but if pressure remains high even after this, then blood volume and flow are altered
Stage 1: compensatory - vasoconstraction and external compression of venous system happen to decrease ICP so ICP during this stage may not change (i.e. no detectable symptoms)
Stage 2: continued expansion of intracranial contents leading to increased ICP, and may exceed compensatory mechanisms. Begins to compromise oxgenation to neurons and systemic arterial vasoconstriction occurs to elevate systemic BP to overcome ICP and promote blood flow to the brain
- transient confusion, restlessness, drowsiness, slight pupillary and breathing changes
Stage 3: Beginning decompensation - ICP begins to approach arterial pressure and brain tissues become hypoxic and hypercapnic; rapid deterioration with decreased LOC, hyperventilation, widened pulse pressure, bradycardiac, and small sluggish pupils
Stage 4: Decompensation - brain tissue herniates (goes from area with greater pressure to lesser pressure) and IICP not evenly distributed; brain tissue even more ischemic and hypoxic
Pyramidal motor syndrome
- involves a series of motor dysfunctions resulting from interruption of the pyramidal system
- injury may be in cerebral cortex, subcortical white matter, internal capsule, brainstem, or spinal cord
- S/S: muscle overactivity - regular excessive movements (clonus and spasms)
- predominantly arm flexors and leg extensors are affected
Coup and Contrecoup injury
Coup: injury at side of impact
Contrecoup: injury from brain rebounding and hitting opposite side of skull
Epidural (extradural) hematomas
Definition, Prevalence, Pathophysiology, Clinical Manifestations, Diagnosis, Tx
Definition: bleeding between dura mater and skull
Prevalence: represent 1-2% of major head injuries, occur in all age groups (most common in 20-40)
Causes/Patho: An artery is the source of bleeding in most epidural hematomas (85%), usually accompanied by a skull fracture; 15% due to injuries to meningeal vein/dural sinus
- Temporal fossa - most common site of epidural hematoma caused by injury to the middle meningeal artery or vein. This causes the temporal lobe to shift medially, causing herniation.
- occasional found in subfrontal area (in young and elderly) caused by anterior meningeal artery injury/venous sinus
- occipital-suboccipital area which results in herniation through foramen magnum
Clinical Manifestations: lose consciousness at injury. 1/3 of those then become lucid for a few minutes to a few days (if venous bleeding)
- As the hematoma accumulates, a headache of increasing severity, vomiting, drowsiness, confusion, seizure and hemiparesis may develop
- Because temporal lobe herniation occurs, the LOC is rapidly lost, with ipsilateral pupil dilation and contralateral hemiparesis.
Dx: CT scan or MRI
Treatment: Good prognosis with early intervention initiated before bilateral dilation of pupils occurs. Surgical evacuation of hematoma usually required.
Intracerebral Hematomas
Definition, Prevalence, Pathophysiology, Clinical Manifestations, Treatment
Definition: bleeding within the brain; may be single or multiple & associated with contusions
Prevalence: occurs in 2-3% of persons with head injuries
Pathophysiology: most commonly located in frontal and temporal lobes. Penetrating injury or shearing forces traumatize small blood vessels. The hematoma then acts as expanding mass, increasing ICP, compressing brain tissue and causing edema.
- Delayed hematomas may appear 3-10 days after head injury
- these hematomas can also occur with non-TBI (like hemorrhagic CVA)
Clinical Manifestations: decreased LOC. Contralateral hemiplegia may occur and temporal lobe hernation as ICP increases
- In delayed hematomas, presentatio is similar to hypertensive brain hemorrhage (sudden, rapidly progressive decreased LOC with pupillary dilation, resp changes, hemiplegia, bialteral positive Babinski reflexes)
Treatement: evacuation isn’t really helpful (only somtimes). Treatment is directed at reducing the ICP and allowing the hematoma to reabsorb slowly
Hypextension injuries of the spine are caused by what forces & result in what?
- results from forces of acceleration/deceleration and sudden reduction in anteroposterior diameter of spinal cord
- lead to fracture/nonfracture injuries with spinal cord damage
- Location of injury: Cervical area
Hyperflexion injuries of the spine are caused by what? What does this result in?
- Results from sudden and excessive force that propels neck forward or cuases exaggerated lateral movement of neck to one side
- produces translation (subluxation) of vertebrae that compromises central canal and compresses spinal cord and vascular structures
- happens in c-spine
Compression injuries to the spine are caused by what mechanisms? Where does this occur in the spine and what does it result in?
- caused by axial loads (from top of cranium through vertebral bodies)
- spinal cord is bruised directly by bone/disk material pushed into spinal canal
- leads to shattering fractures
- injury to T12 to L2
Rotational injuries to the spine are due to what mechanisms? Where in the vetebrae is likely to sustain the injury and what injuries result from it?
- due to shearing and acceleration forces
- happens in cervical spine
- supporting ligaments rupture as well as producing fractures
Herniated Intervetebral Disk
Definition, Causes/risk factors, Pathophysiology, Clinical Manifestations, Dx, Treatment
Definition: displacement of the nucleus pulposus or annulus fibrosus beyond intervetebral disk space. Can occur immediately up to month/years after injury.
Causes/Risk factors: trauma, DDD or both. Risk factors: weight bearing sports, weight lifting, men, highest incidence 30-50.
Pathophysiology: most commonly affected L4-L5 and L5-S1. Ligament and posterior capsule of disk are torn which allows nucleus pulposus to extrude and compress nerve root.
- Radiculitis – compromising the vascular supply and causing inflammatory changes in the nerve root
- may tear entire disk loose which causes disk capsule and nucleus pulposus to protrude onto nerve root or compress spinal cord
Clinical Manifestations: depends on size and location of herniation
- Radiculopathy: disorder of spinal nerve toor. Symptoms associated with pinched nerve from compression/ inflammation - follows dermatomal distribution
- limited ROM of spine/neck, tenderness on palpation, impaired pain, temperature, and touch sensations in the dermatomes affected
Diagnosis: hx and physical exam, spinal X-ray, CT scan, MRI, etc.
Treatment: most heal spontaneously over time and do not require surgery. Surgery if severe compression (weakness or decreased deep tendon, bladder, or bowel reflexes). If cauda equina syndrome then emergency surgical evaluation
Intracranial Aneurysm
Definition, Pathophysiology, Clinical Manifestations, Dx, Treatment
Definition: an bulging in the vessel wall in the brain
Causes: arteriosclerosis, congenital abnormality, cocaine use (causes inflammation to vessel walls and increases BP), trauma, inflammation, vascular sheer wall stress
Prevalence: rupture peak 50-59, postmenopausal women
Pathophysiology: 2mm-3cm. Most located at bifurcations in/near Circle of Willis, vertebrobasilar artiers, or within carotid system where there is higher wall sheer stress and flow turbulence. Can be single but usually more than one present.
- No single pathologic mechanism exists
- Saccular aneurysms (berry aneurysms): occur frequently (but rare in childhood; highest incident of rupturing or bleeding is 20-50 yo) and likely result from congenital abnormalities in tunica media x hemodynamic changes. Sac gradually grows over time and may be (1) round with narrow stalk connect it to parent artery (2) broad-based without a stalk (3) cylindrical.
- Fusiform aneurysms (giant aneurysms): less common and occur due to diffuse atherosclerotic changes & found most commonly in the basilar arteries/terminal portions of the internal carotid arteries
- Rupturing causes hemorrhaging into subarachnoid space that spreads rapidly producing localized changes in cerebral cortex and focal irritation of nerves and arteries
- bleeding ceases when fibrin-platelet plug forms at the point of rupture and as a result of compression & then undergoes reabsorption through arachnoid villi within 3 weeks
Clinical Manifestations: often asymptomatic. Dizziness or headache and cranial nerve compression but depends on size and location. CN III, IV, V, and VI affected most often. First sign commonly acute subarachnoid hemorrhage, intracerebral hemorrhage, or a combo of both/
Diagnosis: arteriography (if before bleeding occurs). If after, then it is based on presentation, hx, imaging
Treatmenet: meds to control HTN and surgery (microvascular clipping or using endovascular coils)
Multiple Sclerosis (MS)
Definition, Prevalence/Risk Factors, Pathophysiology, Clinical Manifestations, Diagnosis, Treatment
Definition: Chronic inflammatory disease involving degeneration of CNS myelin, scarring (sclerosis/plaque formation) and loss of axons
- caused by an autoimmune response to self or microbial antigens in genetically susceptible individuals
Prevalence/Risk Factors: onset 20-40 y.o, more common in women but men have more severe progression. Higher prevalence in northern latitudes. Risk factors: smoking, vitamin D deficiency, Epstein-Barr virus infection.
Pathophsyiology: Etiology UNKNOWN. Autoreactive T and B cells cross BBB and recognize autoantigens, triggering inflammation and loss of oligodendrocytes which typically make myelin. Loss of myelin disrupts nerve conduction with subsequent death of neurons and brain atrophy. Degeneration occurs before symptom onset and happens throughout person’s life. Can also involve spinal cord and cause Spinal MS.
Clinical Manifestations: most common initial sx: paresthesia to face, trunk, limb; weakness; impaired gait; visual disturbances, urinary incontinence. Cerebellar/corticospinal involvement - nystagmus, ataxia, weakness in all four limbs. Tremor and slurred speech.
- Onset, duration and severity of symptoms are different for each person
- Relapses can occur with mild or progressive symptoms (mechanism is related to delayed or blocked conduction caused by inflammation and demyelination). Triggered by trauma, emotional stress and pregnancy
- Recovery from sx during remissions caused by downregulation of inflammation and restoration of axonal function by remyelination, resolution of inflammation or restoration of conduction into demyelinated axons.
- Early cognitive changes - poor judgment, apathy, emotional lability, depression
Diagnosis: hx and clinical exam + MRI. Persistent elevated levels of CSF IgG
Treatment: goal - prevention of exacerbations, permanent neuro damage, and controlling symptoms. Corticosteroids, immunosuppressants, immune system modulators.
- Continuous monitoring required due to increased risk for infection when taking drug therapy
- Plasma exchange
- Supportive therapy - exercise, smoking cessation, avoidance of overwork, heat exposure, fatigue
Primary Brain (Intracerebral) Tumors
Definition: aka gliomas - include astrocytomas, oligodendrogliomas, and ependymomas; makes up 50-60% of alla dult brain tumors
Risk factors: ionizing radiation
Etiology: unknown
Treatment: surgical excission, decompression, chemo, radiotherapy, hyperthermia + supportive therapy to reduce edema
What are fontanelles? Describe the structure and function.
Structure: soft spots on an infant’s head where the bony plates that make up the skull have not yet come together (they are separated at suture lines)
- there are two: one diamond-shaped anterior fontanelle & one triangular-shaped posterior fontanelle
Function: sutures allow for expansion of the rapidly growing brain
- psoterior fontanelle - may be open until 2-3 months
- anterior fontanelle - does not fully close until 18 months
- allows for you to track brain growth (via head growth using head circumference measurement)
Spina bifida includes what forms? Describe each.
1) Anencephaly: anomaly where soft, bony component of the skull and part of the brain is missing. Come out stillborn or die within few days after birth. Dx often made prenatally
2) Encephalocele: herniation/protrusion of the brain and meninges throuhg a defect in the skull resulting in a saclike structure
3) Meningocele: mild form of spina bifida where there is protrusion of the meninges but spinal cord remains in spinal canal
- saclike cyst of meninges filled with spinal fluid and protrudes through the vertebral defect (no involvement of spinal cord or nerve roots)
- develops during first 4 weeks of pregnancy when neural tube fails to close completely; can occur anywhere along spine
- may produce no neuro deficits or symptoms
4) Myelomeningocele: form of spina bifida with incomplete development of the spine and protrusion of both spinal cord and meninges through the skin (postserior arch of a vertebra)
- 80% located in lumbar or lumbosacral regions (last regions of neural tube to close)
Myelomeningoceles are almost always associated with Chiari II malformation (Arnold-Chiari malformation). What is this?
- malformation of the brainstem and cerebellum where the cerebellar tonsils are displaced downward into the cervical spinal canal
- upper medulla and lower pons are elongated and thin
- medulla is displaced downward and may have a “kink”
- associated with:
- hydrocephalus - pressure blocks CSF flow
- syringomyelia - abnormality causing cysts at multiple levels within spinal cord
- cognitive and motor deficits
Congenital Hydrocephalus
Definition: present at birth and characterized by increased CSF pressure
Causes: blockage within ventricular system, imbalanced CSF production, or reduced reabsorption of CSF
Pathophsyiology: increased pressure within ventricular system dilates the ventricles and pushes and compresses the brain tissue against the skull cavity. When hydrocephalus develops before suture fuse, the skull can expand to accommodate and maintain neuronal function
Clinical manifestations: sx depends on cause and extent. Can cause fetal death in utero. Increased head circumference may required C-section.
- Macewen sign/cracked point sign: resonant note sounds when skull is tapped - due to separation of cranial sutures
- Sunsetting - eyes assume a staring expression with sclera visible above cornea
- Cognitive impairment in some
Treatment: shunt or surgery
Phenylketonuria (PKU)
Definition: autosomal recessive metabolic disorder cahractered by phenylalanine hydroxylase deficiency and body’s inability to convert phenylalanine to tyrosine
Pathophysiology: Tyrosine needed for biosynthesis of proteins, melanin, thyrosxine, and catecholamines in brain and adrenal medulla. Accumulation of phenylalanine leads to developmental abnormalities in the brain, defective myelination, cystic degeneration of gray and white matter (leads to mental retardation, hyperactivity, and seizures).
Diagnosis: brain damage has already occurred before detection in urine. Newborn screening used.
Treatment: reducing dietary phenylalanine (PKU diet - low protein)
Retinoblastoma
Definition: rare congenital eye tumor in young children that originates in the retina of one or both eyes
- Two forms:
- Inherited: generally dx during first year of life (40%)
- Acquired: most commonly dx in 2-3 y.o. and involves unilateral disease (60%)
Pathophysiology: Two mutation model of retinoblastoma development - In inherited retinoblastoma, the first mutation is transmitted through the germline of an affected parent. The second mutation occurs somatically in a retinal cell, leading to development of the tumor.
Clinical Manifestations: primary sign - leukocoria (white pupillary reflex aka cat’s eye reflex which is caused by the mass behind the lens). Other S/S: strabismus (red painful eye), and limited vision
Treatment: chemo and restoring useful vision
