Download Neurology - Logan Class of December 2011

Neurology
01-18-07
Pre-Test Given
1. What are the functions of cerebrospinal fluid?
 Primary function is mechanical support—the brain floats.
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9.
Its function is NOT nutrition, if it were it would contain more O2 and more glucose in order to
provide energy for nervous system.
 Acts as a better buffer than alternatives for electrolytes.
 Acts as a pressure gradient when venous pressure changes.
What type of nerve is the slowest conducting nerve?
 C fibers are the slowest they are small demyelinated. C-fibers are
responsible for pain sensation. They fire immediately upon stimulus, but
they take longer to get to where they are going, and they all arrive at
different times, this is why pain often crescendos.
What determines the conduction velocity of each type of nerve?
 The diameter of the nerve fiber, and the presence and amount of
myelination.
 Larger diameter are faster, and more myelination = faster.
What nerve is the efferent loop of the papillary reflex?
 Cranial Nerve 3 parasympathetic division is the efferent loop of the
papillary reflex
Cardinal signs of gaze evaluate what cranial nerves?
 III, IV, and VI
List three modalities carried by the dorsal columns.
 Light touch
 Vibration
 Conscious proprioception
 2 point discrimination
 Deep Pressure
Graphesthesia & stereognosis are cortical functions – they are not carried by the
dorsal columns
Where do the dorsal columns decussate?
 In the medulla
Name the three parts of the brainstem
 Pons
 Midbrain
 Medulla
What is the spinal cord pathway that conveys pain and temperature sensations?
 ALS (anterolateral system) or spinothalamic tract
10. Where does it decussate?
 Crosses in the cord in the ventral white commisure in front of the
canal, therefore in the case of a syringomyelia symmetrical loss is
present
11. What nerve carries sensation to the face?
 Trigeminal, cranial nerve 5
12. Motor control is carried to the face by what nerve?
 Facial, cranial nerve 7
13. Name three parts of the basal ganglia
 Putamen
 Globus pallidus
 Substantia nigra
 Red Nucleus
14. What is another name for the pyramidal tract?
 Corticospinal tract
15. What function does the Eddinger-Westphal nucleus perform?
 Pupillary reflexes—consensual primarily
 Ciliary reflex
16. When is Clonus seen?
 In upper motor neuron lesions – hyper reflexion is the result
17. Where does the lower motor neuron begin?
 At the anterior horn cell
18. Hyper-reflexia without clonus is what grade?
 Grade 3
19. What is the function of the medial longitudinal fasiculus?
 Vestibulo-oculomotor function / pathway reflexes: Car sickness is
problem with vestibular function, proprioception and eyes
Doll’s eye phenomenon – determines brainstem function in unconscious patient –
intact if eyes go opposite of head.
20. What is the middle cerebellar peduncle attached to?
 The pons
Valveless systems:
Batson’s venous plexus
Jugular vein
Oliver Sacks – The man who Mistook his wife for a Hat
Neurology
09-22-05
Neuroanatomy
The average human brain occupies 2% of the human body weight.
Equivalent to 1200 cc
The Cranial vault has a 1500cc capacity
1200 cc occupied by brain
150 cc occupied by CSF (cerebrospinal fluid)
150 cc occupied by blood compartmentalized in vascular tissue
The Brain receives 20% of the cardiac output, and consumes 20% of the available
oxygen. (when you sleep oxygen consumption does slow down some)
The brain requires oxygen and glucose to function. When an individual goes into
acidosis they will survive for a while because the brain cells can burn lactate for a limited
time, but glucose must be restored to continue beyond that.
Oxygen + Glucose = ATP via mitochondria and oxidative phosphorylation. If oxygen
and glucose are not effectively delivered ATP is not made Without ATP various pump
mechanisms (i.e. the Na/K (keep Na out and K in) pumps which maintain membrane
potential to drive neuronal conduction) begin to fail.
Things that alter glucose and oxygen deliver include:
Metabolic acidosis
Due to change in pH secondary to lung or kidney disease, which are
characterized by an impaired buffer system.
Hyperglycemia as in diabetes (same mechanism as above)
Ischemia—less blood
Due to clots,DIC (disseminated intravascular coagulopathy) vasospasm
(migraine), left sided heart failure, aortic stenosis, mitral valve prolapse
(MVP) with or leading to pulmonary hypertension, patent foramen ovale,
tachycardia, Myocardial infarction (MI), Hypovolemia—bleeding out/
Hypovolemic shock, Congestive Heart Failure (CHF) and dehydration
which increases viscosity and thickness of blood, therefore decreasing
delivery. Thickening of the wall of the heart, and arrythmia
All these things cause an increase in heart rate in an effort to push more
blood up to the brain.
Anemias—decreased profusion due to less cells or less iron to attach oxygen to in
order to carry it up to the brain. Can be either from decrease production of blood,
or from blood loss.
Precipitated by poor nutrition, bone disease, genetics, etc.
Decrease in lung expansion decreasing oxygen saturation because of poor
ventilation.
Fever- metabolic demand increases increasing heart rate blood pressure and
respirations.
Kidney or metabolic disease, or colon cancer (due to loss of blood)
Nervous system structures
Thalamus—relay center
All sensory input except smell goes here and is then the thalamus decides
where stuff needs to go and sends it out.
Internal capsule-sensory and motor stuff goes through here—almost everything
Anterior limb- frontal pontine tracts
Genu- corticobulbar pathway from cortex down to the brainstem and cranial
nerve nuclei.
Posterior limb-corticospinal pathway
Motor from cortex to cord to be distributed to the periphery.
Caudate nucleus (superior to the thalamus)- takes care of extrapyramidal activity and
basal ganglion function.
Caudate and putamen together make up the striatum. The striatum is the
biggest input to the basal ganglia receiving information from the cortex.
Movement disorders-those that affect involuntary movements or resting
activities are basal ganglia disorders
The putamen is attached to the globus pallidus, which takes care of output.
The globus pallidus has two parts, interna and externa. The putamen and
globus pallidus together are called the lentiform nucleus.
Parkinsons is a disease of the substantia nigra. (67% of substantia nigra must
be involved before symptoms begin to occur)
Huntingtons is a disease of the striatum (causing choreathetosis)
Hemibalistic problems come from a lesion of the subthalamic nucleus.
Motor disorders that occur with activity involve the cerebellum
Lateral Ventricles- involved in the production of CSF (review CSF function from
previous notes)
CSF is produced at a rate of 20 ml per hour, or 500 ml per day. The flow of CSF
is based on respiratory rates. When you breathe in pressure is decreased, and stuff
is pulled in; when you breathe out pressure is increased and blood is prevented
from draining back in therefore venous and CSF pressures within that closed
system wax and wane.
CSF flows from the lateral ventricles into the third ventricle, then to the fourth
ventricle, then down to the spinal cord. Obstruction between the vault and the
cord lead to hydrocephalus and increased intracranial pressure therefore on a
fundoscopic exam papilledema and choked disc are seen.
Corpus Callosum- allows cerebral hemispheres of the brain to communicate. The corpus
callosum has 3 parts, a body, a genu and a splenium. The Genu (back) and the splenium
(front) do most of the communicating, the body is not as active. This is because of the
genu and splenium having connections with the anterior cingulate gyrus and occipital
poles of the brain and different fasiculi and patterning along brain hemispheres.
Blood Supply
4 large arteries profuse the brain with arterial blood
2 carotids (in front)- come up the anterior part of the neck and into the skull
and provide the anterior circulation (supplies the anterior 2/3 of the brain)
2 Vertebrals (in back)- come up the posterior part of the neck and into the skull
and provide the posterior circulation (supplies the posterior 1/3 of the brain)
In 10% of the population one vertebral artery is vestigial (either smaller
than the other or it is absent.)
As the vertebral arteries come up they join to become the basilar artery.
The basilar artery profuses everything below the tentorium cerebelli (posterior
circulation)
Everything above the tentorium cerebelli is profused by the anterior
circulation.
Posterior Cerebral-supplied mostly by posterior circulation, but receives some retrograde
flow from the anterior circulation.
Occlusion of the posterior circulation
Causes decreased blood flow to the cerebellum and brainstem, therefore an
occlusive disorder of the posterior circulation manifests as cranial nerve
deficiency and cerebellar dysfunction (hypoprofusion of the brainstem)
i.e. dizziness, dysphagia, diplopia, dysarthria
nausea and nystagmus
Long tract signs can also be seen because motor and sensory pathway except
those to the head and neck go through the brainstem.
Anterior circulation- everything above the tentorium cerebelli
Profused by the anterior, middle, and some from the posterior cerebral arteries
Review Homonculus- patients presentation and the geography involved gives us an idea
of what area of the brain or what vessel might be involved.
Coenzyme Q10 can slow Parkinsons by up to 40% by recirculating vitamin E which is an
antioxidant. When taken at 1200 mg per day
Anterior Cingulate gyrus- responsible for pain mediation, mood alteration, executive
function, planning, and organization
Memory goes into the cingulated gyrus where it is then pushed out into association areas
in parietal frontal and temporal lobes for storage.
Wernicke’s area- profused by middle cerebral artery (interpretive speech area)
Broca’s area- profused by middle cerebral artery (expressive speech area) (produces
aphasia and dysphasia)
Internal Capsule lesons can also cause this because all kinds of fibers are compacted
together in this area.
Post limb- profused by middle cerebral artery
Anterior limb- profused by anterior cerebral artery
Genu – profused by anterior and middle cerebral arteries.
Corticobulbar – leads to aphasia and dysarthria (can occur here or
brainstem)
Patient with hemiparetic stroke- has a lesion of the posterior limb or middle
cerebral artery knocking out corticospinal pathways.
Circle of Willis- site of most aneurysms
30% anterior communicating artery
25% posterior communicating artery
5% of the population has intercranial aneurysms (same as percentage with
spondylolisthesis)
The reason aneurysms occur here is because there is no tunica media present at a
bifurcation. If there were and it contracted, it would shut blood off in two directions,
which is bad news.
The circle of willis really doesn’t come into play until a vascular lesion occurs
somewhere else and it is able to provide retrograde blood flow to profuse that area.
Pathways
3 can be assessed with clinical accuracy
Dorsal Columns
Lateral Spinothalamic tract
Lateral Corticospinal tract
Spinal Cord perfusion
Anterior spinal artery- from vertebrals (perfuses anterior 2/3 of spinal cord)
2 posterior lateral spinal arteries also from vertebrals down to T4
Once in thoracic cord branches from the aorta feed the cord
About T9-10 column level the great radicular artery of adamkiewicz perfuses the
lumbar/lumbosacral cord
Important tracts for chiropractors
Vestibulospinal- drive spinal muscles via semicircular canals in cerebellum- reflexive
These can be stimulated with balance exercises to rehab the spine.
Head and neck activities
5 steps of Neurological Diagnosis
1. History and physical- find out whats going on
a. History drives exam, studies, testing, and differential
2. Syndromic diagnosis—determine what if anything as far as symptoms go fit into a
syndrome
a. If yes you have your diagnosis
b. If no move on to step 3
3. Make an anatomical diagnosis- find out where the problem is
4. Etiological- use VICTANE to find the source of the problem
5. Functionality-- find out if it is progressive, static, waxing and waning, will it
resolve spontaneously, will it resolve under your plan etc.
Neurology
09-29-05
5 steps to a neurological diagnosis
History and physical- evaluates cortical function
When you ask a question, the patient has to: hear it, assimilate it, integrate it,
understand it, and then generate a response to it.
Syndrome-what syndrome does it fit into?
Anatomic- find 1 spot that explains everything—not the what part, just the where
Etiologic- finds out what it is, and what is causing it (differential essentiallyVICTANE)
Functionality- how will it resolve? Will it? Or will it get worse”?
Cortical Function:
Verbal Language: controlled by occipital pole
Frontal lobe controls executive function
Don’t just examine on first visit and re-evaluation, examine every time (do the same
thing every time every visit)
This is done so you don’t miss anything
Don’t just settle for the patient saying “I feel better”
3 tracts that can be evaluated with clinical accuracy
Dorsal columns
spinothalamic- crosses in the cord
corticospinal tract
LMN- Hypo- fasciculations
UMN- Hyper
Dissociated sensory loss- in different areas lead to different losses
Associated sensory loss- everything associated with that extremity is lost
Receptors- graded- non-propagated (preceptor)
Receptor potential tested by touch. Signal moves to nerve, then plexus, then
roots, then dorsal horn of cord, then they collateralize into a cord pathway, the go to
the thalamus, then the cortex. Therefore all these areas are evaluated via the sensory
modalities.
Motor stuff: goes from association areas to the basal ganglia, then to the sensory
motor cortex, the primary motor cortex, then the corticospinal tract, to the internal
capsule, the brainstem, the cord, the ventral horn, the nerve root, out through the
named nerve, to the neuromuscular junction and on to the muscle.
Example: 77 y/o male taking coumadin, has small abdominal aortic aneurysm and
presents with weakness in the anterior thigh.
Has patellar hyporeflexia with femoral sensory changes and quad weakness (also
with flaccidity and atrophy)
Lower motor neuron lesion
AAA sometimes leak cause a retroperiotneal hematoma therefore compressing
the femoral nerve
Other modes of Femoral Nerve compression:
Inguinal hernia
Tumor/ mass in colon (right lower quadrant)
Ovarian tumor (unlikely in this case due to gender)
Endometriosis (unlikely due to gender)
With syncope episodes we inspect first:
Head
Heart
Vessels
Vessels is an acronym
V-vagovagal
E-Ectopic Pregnancy = hypovolemia because you bleed out
S-sick sinus syndrome
S-situational
E
L-loss of peripheral vasomotor tone
S- subclavian steel
Cortex
Subcortical structures:
Thalamus
Internal Capsule
Basal ganglia
Cerebellum
Brainstem
Cord
Nerve Root
Named Nerve
Neuromuscular junction
Muscle
Cortical
Evaluate cortical function by watching the patient from the time they are in the
waiting room on. (ambulation, when you walk in the room, etc. all these
things can be commented on in notes)
Include information from the patients history
This tests a great deal of memory- papes circuit (sp?)- recall and
intellectual function
Ask them to remember three objects, ask again later, they should
remember these.
Looking for language, and intellectual function deficits
If they can formulate good sentences, etc.
When assessing deficits also consider educational background, if they
have only gone through 3rd grade, they can do complicated math.
Graphesthesia, stereognosis—higher order functions—processed through the
thalamus
Can only be done based on experience, it has to be something they have
had some experience with.
Subcortical Structures (thalamus and basal ganglia are the two we will worry about)
Thalamus- receives primary sensory and primary motor drive
If not firing on sensory side, primary sensory modality experience is lostwont feel touch pressure, pain, vibration, and we will also lose everything
second order to that. So. . .if they cannot feel the touch of the item in their
hand, they cannot tell you what it is (astereognosis can be cortical or
subcortical—thalamic)
Primary sensory experiences should be assessed first before higher order
functions (dermatomes should be evaluated before stereognosis)
Must be checked thou roughly to determine site of problem (initial
sensory response to neural compression is hyperesthesia, hypo is a
later finding. Same with motor, increased activity is the early sign,
whereas decreased is a late sign)
Ventral anterior nucleus drives cortex for motor systems
Basal ganglia fires to the thalamus to go to the cortex.—you may have
motor losses from thalamic lesions as well as changes of motor integrity
from the basal ganglia.
Basal Ganglia-Parkinson’s (Substantia Nigra)
Tremors at rest
Problems or movement at rest—not a desired activity. Often aberrations
go away once movement is actually initiated.
Cerebellum- easy to assess
Assessment similar to a field sobriety test.
Finger to nose to finger
Stand on one leg
Nystagmus- because fibers of oculovestibular pathway go into the
cerebellum
Etc.
Lack of coordination and clumsiness occur with lesion
Intention tremors, dysmetria, dysdiadochokinesia
Possible signs of brainstem involvement
Brainstem-
Involves cranial nerves and long tract signs.(Dorsal columns,
Spinothalmic, Corticospinal)
Crossed signs of ipsilateral facial
2 cranial nerves reside in the mesencephalon (CN III, and IV)
4 Cranial nerves in Pons (V, VI, VII, VIII)
4 cranial nerves in medulla (IX, X, XI, XII)
V has nuclei in in midbrain, pons, medulla, and cervical cord
Midbrain: sub-serves proprioceptive function for TMJ,
mastication, and extraoculars
Pons: primarily motor for muscles of mastication, and tensor
tympani
Medulla: sub-serves dorsal columns from face and head
Cervical cord: down to C3 in central gray; dorsal horn lamina I, II,
and III –sub-serves pain and temperature from the face and ant.
And middle cranial fossa.
Anterior and Middle Cranial Fossa- headaches (movement
from frontal to occipital happens because the posterior
cranial fossa is innervated by C1, C2, and C3 which means
afferents from the posterior cranial fossa, the back of the
skull and part of the scalp go back into C1, C2, and C3 as
does the trigeminal so they are in the same interneuronal
pool.
Neck: frontal headache
VIII- pontomedullary
XI- two components- medulla and C1-5 Cervical spine componentinnervates the SCM and Trapezius.
Small rootlets come out of C1-5 ascend up to spinal canal back
through the foramen magnum and join the medullary component to
exit the jugular foramen.
Nausea- area postrema in the floor of the fourth ventricle
Medullary component
Dizziness vs. Vertigo
With vertigo the room spins, this involves the semicircular
canals or the cerebellum
Dizziness is a problem with the cerebellum or with
proprioception
Light-headedness is associated with the cardiovascular
system (however watch for long tract signs)
“Judge a Babinski by the company it keeps”
A Babinski Is not always pathologic
It is pathologic when it presents with upper motor neuron lesion signs such as
hyper reflexia, spastic paresis, and clonus
Spinal cord- lesions here demonstrate a well-demarcated sensory level
Very specific level of lesion
Usually initially vascular rather than neuronal
Parasympathetic innervation is only to the core of the body; there is none in
the extremities
Nerve root- lesions cause myotomal or dermatomal losses
Multiple lesion levels are possible here
Disc Injuries- usually occurs in those 20-40 yoa because of physical activity. If a
connective tissue disorders predispose these.
Neurology
10-13-05
acute spinal shock
Transection of the cord- reflexes will be down at first, also initially with a stroke.
Flacidity presents first, then increased ton days to weeks later.
Brain spares itself over everything else
It takes days to weeks for motor changes to occur with a compressed nerve—EMG
changes can occur anywhere from 1-3 days to 3 weeks later.
Case: numbness and tingling in thumb and first finger
Could be radiculopathy, peripheral neuropathy, or plexopathy
If radiculopathy maximum foraminal compression will reproduce symptoms
If peripheral neuropathy the palm will be spared.
Ischemic Penumbra
Normal amount of blood flowing to neural tissue is 55ml/100g/min
When intracranial pressure is increased, blood flow is decreased
Changes to blood delivery to neural tissue manifests in neurologic changes,
such as sensory and motor losses regardless of the cause of loss of perfusion
23ml/100gm/min is the point at which changes (decreased neuronal action)
begins to occur, assuming all other areas of vascular delivery are normal (or in
other words RBC#, HgB, HCT, RDW, MCH, MCHC are all normal)
This is also the point at which EEG waves being flattening (amplitude
decreases)
Neural tissue at this point begins to shut down it is a gradual shut down. (don’t
forget though that at first activity is increased)
Brain swelling, hemorrhage, things that cause increased pressure
55-23 is a large margin for error.
At 12ml/100gm/min isoelectricity (this means there is no membrane potential)
takes place. Because pump fails due to decreased O2 and glucose delivery
there is no membrane potential
Normal membrane potential is –70mV
It is generated by Na/K pumps
Pulls Na out and k in using ATP—this is an energy dependent system
At 6-8 ml tissues die.
Initially there is more activity
Synapse- voltage gated calcium channels
Ca binds to neurotransmitter vesicle to post synaptic membrane and second
order neuron fires
This causes fasiculations (LMNL- nerve root, peripheral nerve, and plexus
only)
If there is no ATP cell energy has to come from breaking down tissues
Increased calcium levels with in neuron activate phospholipase which attacks
cell membranes to generate energy liberating arachadonic acid which reacts
with lipooxygenase and cyclooxygenase to liberate leukotrienes and
prostaglandins (inflammatory mediators) causing swelling and the release of
substance P.
Perfusion decreases as pressure increases
Less O2 and glucose are delivered therefore less energy is
generated and so the pump failure continues.
Scotoma- blind spot
Scintillating Scotoma= wavy lines in the visual field
Fortification spectra=
“Seeing things” comes from increased neural activity—“hallucinations”
These are equivalent from a neurophysiologic standpoint to fasiculations, tingling, or
ringing in the ears.—all increased neural activity
CN 7 & 8 straight out of auditory meatus
Damage here will cause tinnitus—i.e. head injury can cause tethering of the
nerve.
Example (something that causes ischemic penumbra problems): Diabetes- basement
membrane disease- lumen narrowing- with anemia there is even lower vascular delivery.
Anything that changes perfusion causes a problem
Pulse- BP- measures ANS and is driven by the hypothalamus.
Hypercalemia will lead to motor weakness
Artery arteriolecapillaryvenulevein
P-artery> P-capillary> P-funiculus>P-vein>P-tunnel (i.e. IVF, spinal canal)
If this pressure gradient does not exist blood stays in the funiculus (bundle of
nerves)
Change in pressure gradient causes potential failure and loss of perfusion
Minimum necessary perfusion pressure for tissues is 62 mmHg
Autonomics modulate perfusion to the brain through vasoconstriction mechanisms.
When neural tissue cant drain due to tunnel compression blood backs up into the nerve
luckily the nerve is slightly elastic therefore it can give a little when it is squished
O2/CO2 exchange takes place in the capillaries (capillaries have a diameter equal to that
of 1-2 RBCs)
The amount of O2 carried is determined by MCH and MCHC
If there is not much O2 present it doesn’t take long to transfer.
Capillary endothelium is maintained through O2 from capillary blood so when the O2 is
gone the capillary wall tends to weaken, blood then goes through the wall to nerve
funiculus there for mesenchymal/granular/scar tissue forms. Scar tissue has a conduction
velocity of 0. Compression syndrome must be stopped before it reaches this point.—this
is why so many carpal tunnel surgeries fail. . .it is just too late
This all applies to the cord also.
Compression of “Big Tunnel”- by an extramedullary tumor for example
(neurofibroma, meningioma, Blood vessels, hematoma, aneurysm,vascular occlusive ds.,
OA, IVD lesion)
Spinal canal- bordered by Vertebral body, lamina, pedicles
Compression erodes myelin therefore nerve conduction is decreased in velocity therefore
synchronous firing is lost at the end organ because myelin is only lost in certain places.
This also causes sensory dampening, and motor declines
Both of these will come back if pressure is removed before the
compressed schwann cell dies.
The time frame for return depends on the level of compression.
A decrease to 6-8 ml perfusion can cause tissues to start dying within a couple of
minutes.
Spinal cord- no atrophy or fasiculations, --hyper reflexia and increased tone
Re Read Ch5 investigatinal studies
Why would you order these
Also ch5 major motor system disease
The midterm will be 11/3/05
Read Chapter 7 on movement disorders.
Neurology
10-20-05
Emboli- everything downstream will undergo liquefactive necrosis
Valsalva- can exacerbate or cause symptoms of ischemic penumbra
Review/know localization of lesions pgs. 1- 2 of packet
From Chapter 7 Know;
Parkinson’s disease
Basal Ganglia loops
MS
Multiple Sclerosis
Autoimmune disease
2 things are required for someone to come down with MS
1. Genetic predisposition
2. Environmental exposure to agent (agent is unknown)
a. Thought to be heavy metals or viruses
b. The environmental factor precipitates the immune response
causing the body to have a reason to act on mimicking
molecules
Typically ratio= female: male 2:1, 20-40 years of age
can occur later in life but when it does it usually takes on another form
Symptoms: these things are common and can be easy to miss or mistake
Paresthesia- numbness or tingling
Weakness
Clumsiness or lack of coordination
Visual changes
Very little is known about the disease
Geographic Distribution
The further you are from the equator, the more likely you are to have it . If you
move from a low risk area to a high risk area after the age of 15, you fall in the
high risk group, if you move before 15 from low to high risk, you fall in the low
risk group.
In theory—boosting the immune system would make an autoimmune disease worse.
Chiropractic Boosts immune system via autonomic nervous system
For 15-30 min the number of circulating white blood cells increases (there are
not more produced, there are just more circulating)
Gives the WBCs greater exposure to potential pathogens to alert B-cells to
produce antibodies.
Lymphadenopathy in an infectious state is a good thing
WBCs circulate through lymphnodes
Exercise increases the circulation of WBCs too, but is only effective before
getting sick, after you are sick save your energy for body to recover.
Myelin Basic Protein- oligodendrocyte myelin protein
Has peptide strand that triggers and immune response- but you have to have
been exposed to environmental agent (again unknown) to make cells react.
The theory is that Myelin basic protein has a molecular mimicry to some
viruses, therefore after patient is exposed to virus, and body has antibodies, the
body recognizes the myelin basic protein as the virus because it looks the
same.
Vaccines
Activated T cells cross blood brain barrier
Stimulated by immune response (that’s how they become activated)
Tear up oligodendrocyte myelin
The big problem here is that one oligodendrocyte myelinates 20-30
neurons that now have decreased firing to second order neurons
The oligodendrocytes are often lost and are then replaced with astrocyte
proliferation.
Optic nerve, periventricular cerebrum, spinal cord
Colors not as vivid
Activity is increased at first – pressure goes up, perfusion goes down and
hallucinations (visual disturbances) occur.
Visual acuity is affected in 50% of patients
Testing protocol;
MRI
VEP- visual evoke potential- if slow optic nerve conduction is found, it is labeled MS
BAER
4 forms
Relapsing-remitting
Symptoms are in and out going away less each time
Secondary progressive
Relapsing remitting that gets worse
Primary progressive
Later diagnosis—in those 50 years of age or older
Progressive relapsing
Age of presentation dictates treatment
Chiropractic Treatment
Autoimmune
Decrease inflammatory responses
Diet—omega 3 fatty acids- anti-inflammatory
Problem—MS patients have to limit fats (swank diet- under 20 g of fat/ day.)
Huge dietary modifications are necessary with MS
10-27 –05
In class Review for Midterm—questions 1-19, and 41-45 on review sheet
Question 1
a.
b.
c.
d.
e.
History and physical
Syndromic diagnosis
Anatomical diagnosis
Etiological diagnosis
Functional diagnosis
Question 1
I and II are in brain
III and IV- midbrain
V-VIII- pons
IX-XII- medulla
Exceptions: (in addition to above listed)
V- midbrains, pons, medulla, cervical cord
VIII- pons and medulla
XI – cervical cord
Question 3—see packet pages labeled 1 and 2
Also ch.1 of text book
Question 4- intention tremor, ataxic gait, motor trouble with motion, vertebrobasilar
profusion.
Question 5- UMNL- late atrophy
6- LMNL- early atrophy
7.-Peripheral nerve lesion (PNL) vs. LMNL
lmnl= motor
PNL- motor and sensory- will be territorial
Nerve root- dermatomal motor and sensory
Will be affected by spinal motion and patient will have mechanical spine
pain—if not think PNL
8. Neuromuscular Junction (NMJ) lesions
Patient has more trouble later in the day or with exercise (when muscle has
experienced some demand)
More common in small muscles under small demand
Exercise- also increases core temperature so patient declines (uthoffs
phenomenon in MS)
Increased core temp decreases axonal conduction
Autoimmune or inherited
9- symmetric proximal distribution
Most inherited
Consider medications, toxins, solvents, etc.
10- dorsal columns
spinothalamic- crosses in cord, anterior to canal—syringomyelia can mess this up—
symmetric and bilateral—small fibers
corticospinal tract
trauma promotes syrinx formation
15- CSF provides mechanical support, acts as an electrolyte buffer, and has a lymphatic
function
16- Anterior cerebral artery – comes from carotids goes right between hemispheres up to
trunk on homunculus, caudate, putamen, and anterior limb of internal capsule
posterior cerebral
middle cerebral
brocas and wernickes
lateral hemispheres
UE etc. of homunculus
Posterior limb of internal capsule
Vertebral artery- cerebellum, brainstem, cord, (everything below the tent down to T4)
T4- T10 not much going on, perfusion comes from branches of aorta
Lhermttes sign—lightening bolt
Sign of increased activity of dorsal columns with rapid neck flexion into the
extremities and down the back
MS sometimes demonstrates this
41. epidemiology of MS
Female : male ratio = 2:1
Age 20-40
Geographical distribution
Perdispostion + environmental agent required
4 signs and symptoms early- tingling, visual disturbance- optic nerve, weakness must
involve corticospinal or motor pathway
incoordination
MS only involves CNS structures with myelin—therefore not cortex, basal ganglia, or
any peripheral structures—cerebellar cortex.
Oligodendrocytes are lost—astrocytes replace them (granular or scar tissue)
Must be in multiple sites
Periventricular areas- choroids plexus
Plaquing near veins because blood carries immune cells and disease is
autoimmune
Cervical Cord
ALS v. MS
ALS—more typically men 50 yoa +
UMNL and LMNL in ALS
Weakness and atrophy in UE spasticity in LE
ALS—Global relative hyper- reflexia
Fasiculations- LMNL
Cranial and bulbar neuropathy
No plaquing on diagnostic imaging
LMNL
Males 50+
No bowel or bladder loss as in MS
MIDTERM
Neurology
11-10-05
Brain Inury
Craniocerebral trauma
Larger number of brain injured people suffer permanent disabilities of varying
degrees
Tissues to be damaged
Brain
Brain stem
Vasculature
Bone
Head injury- head goes back, brain goes forward onto wings of sphenoid, and cribiform
plate (inferior aspect of frontal lobe) temporal lobe goes under the wings of the sphenoid.
Upon return occipital lobe contacts occipital pole and olfactory nerves that go through the
cribiform plate are sheared.
Age matters- older- cortical atrophy occurs with age which means that the brain shrinks
therefore stretching the bridging veins. These now taut veins under injury tear causing a
subdural hematoma (this isn’t a factor in head injury of a twenty year old)
Causes longterm disability note death ( from a 25 milisecond injury)
Stroke can cause the same thing, short event, long term damage
Head injuries are simple yet complex
Simple because there is no difficulty in determining causation
Complex because of the uncertainty about the extent of injury and delayed
effects
Brain swelling increases intracranial pressure which decreases perfusion and therefore
decreases tissue function as well. Vascular lesion can cause a brain shift
Often seen in patients who strike stationary objects
Concussion violent shaking or jarring of the brain with transient functional impairment
(usually reversible traumatic paralysis of nerve function)
Contusion- a bruising of cerebral tissue without architectural interruption
Mechanism- there must be a sudden application of a physical force of considerable
magnitude to the head
Unless the head is struck the brain suffers no injuries except in the rare instance of violent
flexion extension injury to the neck as in an MVA
Whiplash- formerly called litigation neurosis
Concussion is always immediate
The effects on brain function last for variabl eperiods
Optimal condition is a change in the momentum of the head – acceleration/deceleration
Retrograde amnesia- being knocked out and not remembering the hit because the
pathway was disrupted beforme memory could be stored due to shearing across
mesencephalic-diencephalic eliminates storing of strike memory
Reticular activating system- midbrain connected to the thalamus (????)
Mesencephalon – CN III, IV come from mesencephalon- eye movemnt and
parasympahtetics to the eye for papillary constriction
Pupilodilation seen on side of compresson (temporal lobe herniates down through the tetn
compression CN III)
Can still move eyes at frost because the motor portion of the nucleus is deep
and parasympathetics are in the periphery which is compressed first
The immediate loss of consciousness is the resulty of shear stresses set up by rotational
forces
Maximal shear stress occurs where the hemispheres rotate most easily on the brainstem
This shear stress blocks activation of high reticular formation
Cortical activation is briefly suppressed
Medial reticular formation activity is depressed longer and more severely than the cortex
Effects of concussion
Loss of consciousness
Suppression of reflexes
Falling down if standing
Transient respiratory arrest
Brief period of bradycardia
Fall in Blood pressure following a brief rise
Areflexic (suppression of reflexes)
Pupiloreflex intact
Oculovestibular reflex intact (dolls eye reflex)
Brief babinski because patient is decorticate- mimics lower motor neuron lesion
Patients begin to regain consciousness
Reflexes begin to return
Begin to obey commands and communicate but inappropriately
Memories are not formed during this time
Recovery time varies from minutes to days
Because we don’t know how much damage occurred or how much damage
was already there
For the patient the period of unconsciousness extends from a point prior to the injury
(retrograde amnesia) until consecutive memories can be formed again (anterograde
amnesia)
The duration of the amnestic period
Minor head injury
Two degrees of disturbed function
Stunned- saw stars
Consciousness is temporarily abolished
Effects recovery
Greater risk of tissue injury
Post Injury Sequelae
Delayed fainting after head injury
Drowsiness, headache, and confusion
Transient traumatic paraplegia, blindness, or migrane phenomenon
Delayed hemiplegia or coma.
Neuro
11-17-05
Post- Injury Sequelae
Delayed fainting after head injury
Vasodepressor syncope
Due to pain and emotional upset
Must consider other causes
Intracranial bleed
Brainstem injury
Lucid interval- period of consciousness between two periods of unconsciousness
Hypoxia/Hypoglycemia
E-epilepsy
A-Anxiety
D-dysfunction of brainstem
H- heart attack
E- Embolus (pulmonary usually)
A-Aortic Stenosis
R- Rhythm dysfunction
T- tachycardia- usually ventricular
V- vaso-vagal
E- Ectopic pregnancy
S- situational
S- sick sinus syndrome
L- loss of peripheral vasomotor tone
S- subclavian steal
Hypoglyemia/ Hypoxia- failure of O2/glucose to be delivered to the brain.
Endocrinopathies, anemias, etc.
Epilepsy- create changes in levels of cortical activity
Anxiety- autonomic efferents driven up by stress resulting in failure to perfuse
D- dysfunction of brainstem- cardioregulatory and vasomotor governed by autonomic
systems in the brainstem—changes blood pressure, heart rate, vasomotor tone
Heart attack- stroke volume decreased due to heart failing to function
Embolus- pulmonary- decreases gas exchange leads to hypoxia
A-aortic stenosis- decrease perfuion- via dissection or hypertrophic septal changes
R- rhythm dysfuntion- can’t get enough blood into the heart or blood to the brain
T- Tachycardia- heart moving too fast to move blood to brain
V-vasovagal=situational= anxiety
Limbic system drives autonomics
Ectopic pregnancy- hypovolemia- unrelenting abdominal and back pain- tube can rupture
and causes bleeding out
½ pulse pressure + diastole
Situational
Sick Sinus Syndrome- cardiac rhythm
Loss of Peripheral vasomotor tone- decrease in BP= no perfusion to brain
S- subclavian steal- vaso-occulusive disease of upper trees and do upper extremity
exercise so blood is shunted to UE so in brachiocephalic trunk goes more brachio than
cephalic and grandma drops due to decrease perfusion.
3 complications
dizziness
light headedness
vertigo
Vertigo- something has to spin (either patient or room)
Most commonly semicircular canals, ocular, proprioceptive
Dizziness- unsteadiness with out spinning
Proprioceptive – sensory or motor
Light headedness- cardiovascular
Knocked out= brainstem because reticular activating system in the brainstem
Drowsiness headache and confusion
Most common in kids
May include vomiting (increased intracranial pressure – nausea, vomiting,
papillary changes)
May appear as intracranial bleed
Usually subsides after a few hours
Transient traumatic paraplegia, blindness or migraine phenomenon
Depends on site of insult
Paraplegia may include incontinence w/ bilateral babinski
May be a result of blows to top of head or C spine injury
Blindness from occipital region injuries
Followed by vascular headache and symptoms
Momentary dislocation= cord bump=syringomyelia formation later on
Delayed hemiplegia or coma
Seen in young males after minor injuries
Develop hemiplegia, hemianesthesia, homonymous hemianopsia, or aphasia
Neck injuries, can cause neural thrombosis and carotid
May be latent effect from intracranial bleed
Concucussion followed by lucid intervals
Acute epidural hemorrhage
Acute or chronic subdural hematoma
Cerebral contusion
Intracerebral hemorrhage
Acute epidural hemorrhage
Usually due to temporal or parietal fracture that damages middle meningeal
vessel
May be venous sinus tear
A few hours later complaints are
Headache with increasing severity
Vomiting
Drowsiness and confusion
Coma
Acute and Chronic subdual hematoma
Acute
Brief lucid interval from injury to coma
May be combined with epidural hemorrhage
Chronic
Traumatic etiology unclear
May have been a trivial injury (elderly and anti- coagulation patients)
Headaches and slowed thought or confusion
Hemiparesis and occasional aphasia
Papillary dilation is important indication of site
Post-traumatic nervous instability
Post concussive syndrome
Troublesome and frequently encountered
Headache is a central symptom
Ache, pound, throbbing, stabbing, intensifies with phyical/ mental exertion
Dizziness but not ture vertigo- looking up or to side increases dizziness
Intolerant of noise
Restless
Unable to concentrate
Fatigue
Apprehension and worry
Alcohol intolerance
Insomnia
Chronic Inflammatory process
12-1-05
seizures
generalized vs. partial seizures (ch. 8)
Strokes Ch. 9
Pay attention to risk factors and family history
Acute or abrupt neurologic situation with duration greater than 24 hours
Under 24 hours it’s a TIA- transient ischemic attack
Risk Factors
Hypertension (obesity, poor exercise, other contributors)
Hyperlipidemia or dyslipidemic syndrome
Hemoglobinopathy- sickle cell anemia, thalasemias,
Smoking- causes vasoconstriction and decreased oxygenation
Oral contraceptives
Medication
History- cardiomyopathy, cardiac events, atherosclerotic disease, atrial
fibrillation
20-25% of strokes are cardioembolitic features
Strokes
1 of 2 events, either ischemia or hemorrhage—ischemia represents a block, hemorrhage
represents a rupture.
Ischemia can occur 2 ways
Thrombosis
Embolus
Thrombosis- long development
Ultra sound at carotid bifurcation done after stroke
Most common disease segments of the vertebral artery are at C6 and C1/2
Different symptoms indicate a problem in different areas
Typically stroke patients don’t regain fine motor control
TIA= warning sign—80-85% progress to a stroke within 5 years
Multiple TIAs in the same place indicate a thrombus
Narrowing one vessel opens another allowing for retrograde flow
Thrombus is milder than an embolus
Embolus- shuts vessel down – abrupt onset TIA that resolves then another at another
place, then another. . . = showers= multiple emboli= cardiac.
Ant. Vs. post. Circulation
CT ordered – sensitive for proteinacious fluid
Rules out intercranial bleed
If bleed is ruled out and patient is within 3 hours of onset clot buster meds can be given—
streptokinase, TPA