NEUROLOGY – 5/15/08
*** 2 EXAMS…Midterm and Final…Midterm is 50/50 (short answer and fill in the blank) and so is the final (same
format)…Sometimes he’ll take attendance more often early in the trimester ***
Initial Screening of the Nervous System by Use of Vital Signs
1st thing you do to evaluate nervous system during a physical exam is to take a pulse (pulse is driven by ANS). The second
thing to check is BP. BP is also driven by the autonomic nervous system (ANS).Start with the simplest of tasks and progress
from there. Rapid pulse can mean sympatheticotonia.
Cardio regulatory function is under joint influence by autonomics and self regulatory mechanisms.
Stress and Vitals
Stress can affect the pulse rate. Stress is linked with memory. Stress is based on an emotional event due to memories made to
exposure to a ―stressful situation.‖ An example would be a scent that triggers a memory. The memory then creates a
psychological and physiological response of increased pulse rate and blood pressure.
If you argue that chiropractic boosts the immune system and good chiropractic care will help immune response, then be
prepared with the question why do you treat patients with autoimmune diseases with a functioning immune system. The
immune system is functioning normally, attacking what it sees as foreign material.
Stress can trigger the hypothalamus to fire. The limbic system is often involved and associated with hypothalamic firing. The
response is to increase BP, stimulate the release of releasing hormones via portal system, increase heart rate and increase
Physiological Changes with Hypoxia
State of hypoxia can be measured by electrolytes in the blood, pulse rate increases, breathing rate increases, temperature and
pH changes. Other changes are that room oxygen levels go down, oxygen levels in the blood go up, hemoglobin will go up to
carry more O2 serving as compensation for a hypoxic state.
Example of Rectal Bleeding, How it impacts the Body and the Body’s Compensation
Ex. -- After the age of 50, colonoscopy is recommended to check for polyps (pre-malignant). Polyps can bleed silently. This
can lead to anemia. Anemia changes pH and O2 concentration. The change in pH and O2 concentration triggers the
hypothalamus, breathing centers and pulse centers. The response is that you can breathe more quickly and send blood more
The Effect of Ischemia and Hypoxia
Lack of O2 can lead to decreased oxidative phosphorylation. ATP production drops. The sodium potassium pump fails. We
now get closer to threshold creating either sensory or motor problems. The process is broken down as poor oxygenation of the
tissues leads to failure of the pumps putting the condition closer to threshold. Less stimulation is needed as the nerve is closer
to threshold creating sensory or motor problems. The situation eventually leads to numbness and tingling or motor problems.
Summary of the Ischemic Process
1. Change in pH and O2 concentration occurs with ischemia
2. Decreased O2 leads to slow down of oxidative phosphorylation.
3. Decreased Oxidative phosphorylation decreases the energy produced (ATP)
4. Lack of ATP affects sodium/potassium pumps
5. The sodium/potassium pumps fail and we get closer to threshold (either sensory or motor)
6. Bringing the nerve closer to threshold makes the nerve excitable and causes firing (pins and needles sensation in
sensory nerves…..OR…fasciculations/muscle firing in motor nerves) – less stimulation is needed
7. Eventually the nerve is hypoesthetic (doesn’t respond) as the ischemic/hypoxic state remains
8. Eventual numbness or motor problems result
The situation is self-perpetuating as hypoxia leads to tissue damage. Tissue damage leads to inflammation that requires
greater demand for oxygen and nutrients. The demand cannot be met and the hypoxic/ischemic state worsens creating
Veins are compressed first with an SOL, not nerves. Disc Herniation impacts a confined space. Volume stays the same with
an SOL but contents and pressure both increase. Pressure occurs first on the low pressure venous system and causes a backup.
Venous blood backs up into the nerve funiculus (connective nerve tissue). The connective tissue decreases in AP and vertical
dimension setting up in a poor drainage situation. The elastic tissue allows expansion for a limited amount of time. If the
build up remains, the capillary bed will back up. The capillary is responsible for exchange. The back up decreases the
capillary’s ability to exchange and causes O2 to decrease (hypoxia). The hypoxic state then leads to the hypoxic/ischemic
pathway of affecting oxidative phosphorylation, decreasing ATP, and eventually leads to numbness and tingling.
The venous system is prone to compression with an SOL. If the system remains occluded, it can lead to the
ischemic/hypoxic pathway by backing up the capillary bed.
Reticular Activating System
―Knocked Out‖ – The spinal cord is tethered at the bottom (pia mater to sacrrococcygeal ligament. You’ve also got denticulate
ligaments that further tether the cord. As the bran moves everything moves with it; however, the tethering of the cord restricts
that motion. The movement and restriction to movement creates rotational shear forces that pulls at the midbrain and RAS.
The midbrain is the location of the Reticular Activating System (RAS). In boxing, rotational shear stress knocks someone out.
Rotational shear stress is the culprit for getting knocked out.
Practice Test Questions
1. What are the functions of CSF? Lubrication (decrease friction), Protection, Buoyancy (mechanical support),
Nutrients (electrolyte buffer – doesn’t provide electrolytes but is a buffer), Lymphatic Function…CSF should have
the same concentration as serum. CSF does not carry O2 and should not have glucose or cells in it. It is a buffer for
electrolytes. CSF has a lymphatic function.
Space occupying lesion can be provoked by Valsalva. The lesion is typically in the canal. Tumor, herniated disc and others
pathology are causes for the SOL.
Ex. Patient presents with pain in back, problems bearing down, radicular type pain. Radicular pain occurs because of venous
occlusion. Bearing down increases intrathecal pressure within the meninges (increased CSF pressure). Bearing down
creates pressure in thoracic cage. Blood is backed up through the venous system. There are no valves in most veins,
including the jugular veins. Increasing intrathoracic pressure backs up the jugular veins. The back up affects the
venous sinuses in the cranial vault. The sinuses fill with more blood and expand. The head is a closed vault and can
only take a limited volume. Pressure is transmitted by the foramen magnum and CSF which creates pressure down the
spinal column and cord. The pressure creates the mechanical irritation necessary to have a “true pinched nerve.”
Mechanical irritation forces depolarization bringing the nerve closer to threshold causing firing. The firing presents in
Vomiting helps relieve cranial pressure.
#2.What type of nerve is the slowest conduction nerve?
#3.What determines the conduction velocity of each type of nerve?
Diameter of the axon and myelin determine the conduction velocity.
#4.What nerve is the afferent loop of the pupillary reflex?
Optic nerve (CN #2)…You don’t have to have conscious perception of light to have the reflex
#5.Cardinal signs of gaze evaluate what cranial nerves?
CN 3, 4, 6
#6.List 3 modalities carried by the dorsal columns.
D-Touch/Light Touch, Vibration, Proprioception on the conscious level, Pressure, 2 Point
The widest gap of 2 point is the back with the smallest is the tips of the 2nd finger.
Gravesthesia and Stereagnosis
Gravesthesia = Draw a letter on a body part and see if the patient can recognize what you drew. If the patient can’t recognize
the letter, it may not indicate a lesion, but could indicate the patient does not have the sensory experience and memory to know
what letter you drew (ex. They could be illiterate). The cortex is responsible for recognition, which is a function of memory.
Gravesthesia and stereagnosis involve the cortex and memory. Be aware of this when you test these 2 modalities.
#7. Where do the dorsal columns decussate?
They decussate in the medulla (internal arcuate fibers). Important to know because you have to know where the lesion is
at. Is the lesion dorsal column, nerve root or above the decussation. If the lesion is above the decussation the presentation is on
the opposite side. If below the decussation, the lesion is on the same side.
#8. Name the 3 parts of the brainstem?
Medulla, pons, midbrain
#9.What is the spinal cord pathway that conveys pain and temperature sensations?
#10.Where does it decussate?
At the cord level within 1-2 segments
#11.Sensation to the face is carried by what nerve?
#12.Motor control of the face is carried by what nerve?
Facial and Trigeminal
#13.Name the three parts of the basal ganglia.
Caudate, Putamen, Globus Pallidus (Interna and Externa)
#14.What is another name for the pyramidal tract?
Corticospinal Tract vs. extrapyramidal (movement when you don’t want it-resting tremors of parkinson’s)
Cerebellar disease you have more movement than you want. Modulation of movement is where the cerebellum comes in.
Undesired movement at rest is a basal ganglia problem
#15. Where does the lower motor neuron begin?
Ant. horn cell or 2nd order neuron…Sensory has 3 neurons and motor has 2 neurons.
#17. When is clonus seen?
Upper motor neuron lesion is evident in hyper-reflexia. The nervous system is closer to firing due to lack of inhibition.
Putting a stretch reflex into the system will generate a stretch reflex occurring between flexors and extensors (clonus). The
lack of inhibition makes this possible. Clonus is easier to see in the wrist and ankles.
#18. Hyper-reflexia with transient clonus is what grade?
Components of UMN is hyper-reflexia, hypertonic muscles, decreased strength, Babinski sign and clonus. It is possible to
have a Babinski sign without some of the other manifestations, so make sure you consider this when making a diagnosis.
#19. What is the function of the medial longitudinal fasciculus?
Vision and balance
Move head one way and eyes go the opposite way. Move head to R and eyes go L. Tilt head down and eyes go up.
COWS—Cold Opposite and Warm Same---Caloric Testing
To test the fasciculus, take an ear syringe and squirt it into an ear. It causes the endolymph in the canals to slow its movement.
There is discrepancy between each side of endolymph L vs. R. This drives the eyes to the irrigated side ear. Causing
nystagmus. Nystagmus occurs to the fast side. The sense is that the head is moving one direction and the eyes drift to one side
slowly followed by a response to the opposite side quickly. Cold opposite tells us the system is intact.
We then flood the other ear with warm water. The nystagmus should drift to the same side (warm same).
Caloric testing affects the midbrain-pons-medulla and hypothalamus. This is where the deep centers for consciousness and life
#20.What neural structure serves to control both neural and endocrine function?
VICTANE or VINDICATE—Used to form differential diagnosis. Possibilities = less than 50%...Probablities = Greater than
NEUROLOGY – 5/22/08
Pain & Where is the Lesion
Theories on Pain
Gate control, Central Biasing Mechanism, Psychosomatic, Endogenous Opiate
The Importance of Making a Correct Diagnosis
Ex.—Midback pain…In this example, the patient has a slow stretch in paraspinal muscles, causing contraction via the creep
mechanism. This increases muscular demand. The demand is not met due to decreased perfusion. Decreased perfusion leads
down the anaerobic pathway (an inefficient pathway to generate ATP). The pathway leads to metabolite build-up of lactic acid
and leads to further problems.
The adjustment gets rid of pain, but in this scenario the patient comes back. You adjust them again, they get better, and the
process continues. So ask yourself, is your diagnosis correct? That is a reason why a full physical exam is necessary on the
first visit. This is an error of omission and commission….You can adjust the patient for the pain, but until you identify the pain
generator you cannot properly manage the situation and may be liable by omission and commission.
Pain can be sent to the midback by many structures (esophagus, lung, gallbladder, etc.)…
Identification of the Problem
Identification of pain is felt at the level of the somatosensory cortex. You must identify the source of the problem to lead to the
path of proper treatment.
Limbic System works through an expectation based on a recollection of a previous event. Ex.—You get a headache from an
adjustment….The next adjustment you expect a headache. The limbic system remembers the event and activates the reticular
formation and hypothalamic drive. Pulse goes up, BP goes up, and stress hormones go up. You’re thinking I’m going to get
hurt, and you think I’m going to get worse following the adjustment. So this is a limbic event.
Stress and limbic events can go hand in hand. Don’t ignore the limbic system. Patient expectation and pain expectation are
important. Changes in the limbic system occur due to memory and learning. Under stress you don’t learn, you are in catabolic
state and can’t make neural connections.
Make Linkages and associate different receiving signals to put them into a cohesive experience for you to draw upon.
MOTOR AND SENSORY
Motor, Initiation of Movement and Motor Programs
Primary Motor and Sensory Cortices
The desire to move must come from a conscious thought about movement (cortex). The association cortices drive movement.
Ex. You want to pick up a piece of paper from the floor…First you must have a desire to pick up the paper. Second, the
association cortices must fire in the brain to start the process of movement. The program for movement is stored in the basal
ganglia (all motor programs are stored in the basal ganglia). The basal ganglia fires to the thalamus (ventral anterior
nucleus of the thalamus). The VAN nucleus allows the thalamus to activate the cortex. The message goes to the supplemental
motor cortex (association cortex). The association cortex fires back to the primary motor cortex. The primary motor cortex
will send the message down the corticospinal pathway to begin movement. Through the corona radiate, then the internal
capsule and goes into the brainstem. From the brainstem, it goes to the pons and transverse pontine fibers. The path crosses
via the middle cerebellar peduncle into the cerebellum. The cerebellum gets the message that this is the movement I want to
perform and it is the cerebellum’s job to make the movement smooth and coordinated. The cerebellum has the information for
what the muscles and joints want to accomplish. The motor pathway crosses at the medulla (part of the message goes to the
cerebellum and part of the message heads to the medulla) and goes down the cord. It leaves the cord out the root. It later heads
to the plexus, and to a local nerve to the agonist and antagonist muscles.
Recap of movement – how conscious movement begins
1. Desire to Move
2. Firing of the Association Cortex to begin the sequence
3. Firing heads to the basal ganglia where the motor program is stored
4. The message heads to the thalamus (VAN – ventral anterior nucleus)
5. Thalamus activates the motor association cortex
6. The association cortex fires back to the primary motor cortex
7. The primary motor cortex sends the message down the corticospinal pathway
8. The message travels through the corona radiata, internal capsule and into the brainstem
9. The message goes into the pons and transverse pontine fibers
a). Part of the message then goes in the cerebellum via the middle cerebellar peduncle. The cerebellum
makes the movement smooth and coordinated.
b). Part of the message heads to the medulla and crosses
10. The message that traverses the medulla heads down the cord leaving at the nerve root.
11. The message travels through the plexus to a named PNS nerve to agonist and antagonists (specifically, the
12. Electrolyte release and neurotransmitter release trigger a movement.
Children and Motor Programs
Children do not have the capacity to perform the same tasks as adults. One reason may be that they lack the proper motor
program within their basal ganglia. The program allows the child to execute the movement, like a computer can execute a
command through use of a program
Ex…A kid picking something up….The child cannot pick up the toy because they cannot grasp it. The child stares at the toy
and slowly moves towards it, but doesn’t have the program and cannot execute the grasp quite yet. The child must build the
motor program by combining the visual information, sensory stimuli, and the urge to grasp.
Cortex Vs. Basal Ganglia
If you let the cortex run the show, you’ll overcorrect and screw things up. If you learn the motor pattern and trust the motor
program, you can do the event faster and better. We see this in athletes that have repeatedly trained to store and execute the
motor program. AS a result, they can perform the same given task faster and more efficient than an average person can.
The motor system does not function alone. Information from the periphery is required to influence the cerebellum and the
Alcohol’s Impact on the Cerebellum and Motor Function
Alcohol disturbs the cerebellum impairing the motor control system. In a field sobriety test, they check cerebellum function.
Walk heel to toe, follow my finger, stand on one leg and count are examples of checking sobriety and cerebellar function. The
cerebellum coordinates motor control with sensory input to get a desired result. Alcohol impairs the ability to get the desired
Motor Programs and Motor Learning
We learn motor functions and motor control by making proteins via our genetic code. The proteins are made when we learn.
We learn based on environmental experiences. Each person has different abilities to learn based on genetics and experience.
Executive Function of the Frontal Lobe
Prefrontal Association cortex
Frontal lobe is good for executive function (planning, organization, thought) and is where most cognition occurs. The superior
and inferior longitudinal fasciculus are fibers that take info from visual and auditory cortex (temporal) to the frontal cortex.
We recognize the image and send the message to the frontal cortex so that we can interpret what the heck it actually is. The
same occurs with auditory information.
Unimodal Association Areas
1 variety of signal is discerned
It is important to note that when localizing lesions…The homunculus is a representation of the body on the brain. These areas
are affiliated with sensation or movement.
Dermatome Testing – What is actually checked when you test dermatomes?
Dermatome Testing Affects: 1). Receptor 2). Local Nerve 3). Regional Nerve 4). Plexus 5). Spinal Cord (Dorsal Columns) 6).
Integrity of the pathway within the cord (through medulla – crossing --- heading to thalamus) 7). Thalamus (ability to let
message get to the cortex) 8). Cortex (ability to recognize where the stimulus is from)
Ex. L5 dermatome…Do they feel the same side by side? What do we check? We check the ability of the receptors to
transducer (taking mechanical information and converting it to a electro-chemical signal). We also check the local nerve,
common peroneal nerve and axons of the nerve. We check the sciatic nerve. We check the lumbosacral plexus. We check the
cauda equinae. We check the spinal cord and the dorsal columns. We check the message as it heads through the medulla,
crosses, heads into the thalamus and then to the cortex. We check the whole pathway from toe to brain on both sides.
If you can’t feel it, we don’t know exactly where the lesion is! This is why we check multiple sensory modalities. We check
multiple modalities to help identify the different receptor types. Pain and temp are both spinothalamic pathways but need
Myotome Testing – What is actually checked when you test myotomes?
The same occurs with the motor systems as the whole pathway is checked…Ex. Weakness in elbow flexion, could mean
problem in the motor cortex, problem in the internal capsule, problem in the spinal cord, nerve root, plexus, the muscle or the
NM junction. We don’t know unless we further test.
Sensory Changes – Numbness and Tingling
Numbness and tingling is an increase in neuronal activity (excitation). Initially the nervous system is hypersensitive .
Hypoxia triggers the hypersensitivity and the increased level of activity. Numbness and tingling due to hypersensitivity
is the first response to hypoxia.
Suspected carpal tunnel tested by Phalen’s may yield a + result of numbness and tingling. You have to be able to feel the
change first. The entrapment of the median nerve occurs. The entrapment is felt and perceived by the body as numbness and
tingling. Numbness and tingling occurs because of hypoxia due to hypersensitivity, linked with venous stasis/swelling.
Physiological Reserve, Decreased Blood Supply, Hypoxia and Implications of Venous Stasis/Swelling
Normal blood supply is 55 ml/100 grams/minute. We can sustain a 50% decline in blood supply (25
ml/100grams/minute) before we sustain damage to neurons (especially cortical neurons). We will see decreased activity
EEG’s and EMG’s when reserve hits 25ml/100grams/minute. The initial response to decreased blood supply is
hypersensitivity with increased levels of firing and increased activity.
Ex.. Checking dermatomes….The patient reports, ―I don’t feel that as much.‖ Is that because you don’t, or you feel the other
side more? You need to check other areas to help establish a baseline. The initial response to neural compression is increased
activity. If the compression continues, the nerve tissue becomes iso-electric. At 12 ml/100grams/minute we become iso-
electric and lose the potential of the membrane. The nerve will not conduct, but it is not dead. It is possible the nerve
will recover when it first turns iso-electric.
Chart of Blood Supply
1. Normal: 55 mL/100 grams/minute (less than 55 mL and we see hypersensitive/excited patterns
of numbness and tingling or fasciculations)
2. Decreased: 25 mL/100 grams/minute – Damage to neurons occurs with decreased activity
3. Isoelectric: 12 mL/100 grams/minute – Nerve does not conduct, but is not dead. Loss of
The numbness and tingling initially is the nerve firing on its own. Stopping of numbness and tingling may be good or bad, but
you need to check. Lack of numbness may indicate the condition is progressing, or it may indicate the situation is getting
better because of lack of numbness. The key point here is that you need to examine the patient!
Ex…Migraine headaches often have vasoconstriction which gives patient’s the aura associated with true migraine headaches.
Decreased blood flow decreases O2 and induces a state of hypoxia. Hypoxia decreases ATP generation and increases
anaerobic pathways. Decrease ATP with increased use of anaerobic pathways causes decreased activity of the NA-K pump.
Further changes occur when the pumps don’t function.
Ex. Fasciculations…Muscles that twitch. A small group of muscles is a fascicle. Inter-compartmental pressure changes affect
ATP generation leading to the twitch. The twitch is a result of excitation of the nervous system due to decreased blood flow
Sensory and Motor Disturbances
We think of them as separate, but we are finding integration between loss of sensory and loss of motor. A common finding is
that hypoxia can trigger either sensory or motor changes.
Numbness and tingling can present with migraines. The process starts with: 1). Vasoconstriction 2).Hypoxia and 3.).
Hyperexcitability (aura, ringing in ears, visual disturbances). The vasconstrictive phase can impact the cortex. If the visual
cortex is affected you’ll see things that aren’t there. If the auditory cortex is affected, you’ll hear things that aren’t there or
The location of vasoconstriction impacts what signs and symptoms present first. Visual auras are not necessarily the visual
cortex. Vascoconstriction can occur anywhere along the optic nerve, association area, or at other places in the visual pathway
generating the aura. The same is true for the auditory system.
Slow cord changes, we have the ability to adapt (ex. Elderly people with spinal stenosis can remain quite functional for long
periods of time). In acute changes, we may not have the ability to adapt ( ex. disc herniations – patients can lose sensory and
motor very quickly).
It never occurs. When you tap the tendon, you have to trigger the agonist and dampen the antagonist. You fire the alpha
motor neuron of the bicep and have to release GABA in the antagonistic pathway to inhibit the tricep. In actuality, the other
side has to move as well (if you test the right, you will also fire the left). This is because of cross-crawl reflexes.
Stroke Rehab & Mirror Imaging
If you touch your nose, the person viewing you will fire their brain. The person doesn’t actually perform the movement, but
their brain fires the motor pattern. In stroke rehab, put them in front of a mirror and have them watch their motor performance
so that their brain relearns the motor pattern to the opposite side. In stroke patients, you have to rebuild the cortex to fire to the
pathway, so by looking in the mirror they can visualize the opposite arm moving, this is voluntarily tricking the brain to relearn
the movement pattern.
It is the same thing with phantom leg syndrome in amputees. The goal is to stimulate mechanoreception to blocking the pain
generated at the level of the brain by the amputated leg.
Middle Meningeal Artery
Epidural Hematoma: Bleeding that can kill someone…It can happen in auto accidents and in contact sports.
Ascending vs. Descending Pathways
These are the only 3 we can test with certainty!
Ant. Spinal artery comes of the vertebro-basilar system. The 2 posterior spinal arteries perfuse the dorsal columns. The spinal
cord is about the size of your index finger/thumb.
Description of Rexed Lamina and Function
1 & 2: Nociceptive (primarily #1).
3 & 4: Mechanoreception
5: Nociception (nociception is pain that is not yet consciously perceived. It is just a sensation that is noxious
and different from mechanoreception)
7; Autonomics (5 fees into 7, so autonomics are impacted by nociception)
8 – 10: Motor
NEUROLOGY – 5/29/08
ANATOMY AND VASCULAR SUPPLY TO THE BRAIN
Adjustment and Pain Control
Mechanoreceptive drive will inhibit nociceptive input. Information from nociception comes from Rexed laminae 1 and 2.
Mechanoreception comes from 3 and 4. Mechanoreception from Rexed laminae 3 and 4 head back to inhibit 1 and 2. The info
goes to the dorsal horn and stops there because mechanoreceptive drive inhibits nociception, stopping pain in its tracks. An
adjustement is theorized to help stimulate mechanoreception and therefore decrease the ability of pain to be transmitted to the
brain, hence the patient can experience decreased pain.
Ex. Rubbing the area of pain…Rubbing it stimulates mechanoreceptors at the dorsal horn blocking pain.
Effect of Ant-ipsychotic and Anti-Depressant Drugs
A lot of antipsychotic drugs affect the basal ganglia and motor control systems. If you inhibit the globus pallidus, you can
cause dis-inhibition (dis-inhibition is actually activation since the removal of the inhibition causes activation). A lot of anti-
depressants, anti-psychotics will generate problems in the basal ganglia. A side effect is changes in BG activity. Anti-
psychotics change BG activity and release the thalamus, thus activating the cortex triggering involuntary movement.
Arterial Supply to the Brain
Anterior Circulation, Internal Carotids, Everything Above the Tentorium Cerebellum
You need to remember the tentorium cerebelli as a border. Vascular delivery systems can be divided at the tentorium cerebelli.
We have anterior and posterior circulation to the brain. Anterior circulation comes up the internal carotids. With small
exception, everything above the tentorium cerebelli, gets vascular supply from the internal carotids (this is termed ant.
circulation). The Ant. and Middle Cerebral arteries come from internal carotids.
Posterior Circulation, Vertebro-Basilar System, Below the Tent
Posterior Circulation is the vertebral basilar system that perfuses everything below the tent. The cerebellum is located
below the tent. The cerebellum through 3 peduncles is attached to the brainstem. The inferior cerebellar peduncle is attached
to the medulla. The medulla is above the FM (foramen magnum). The brain stem in normal individual does not extend below
Consistency of the Brain
Brain consistency is like pudding. It is made of fat. Myelin is made of fat, hence brain is fat.
Uniqueness of the Trigeminal Nucleus
Trigeminal nuclear complex runs below the FM going down to C1-C3 area, so sensations from the face go down to the nucleus
located in the cervical, before being sent back to the brain for interpretation.
Below the Tent
The cerebellum and the brainstem are located below the tent. The area below the tentorium cerebellum is perfused by the
vertebro-basilar system. The ant. spinal artery and the post. spinal artery branch the VB system.
Poor perfusion can cause problems like vertigo, dizziness (8th cranial nerve – off the brainstem), hearing loss ( 8th cranial nerve
of the brainstem). A decrease in perfusion from 55 mL to 25 mL causes sensory changes.
Importance of Locating the Source of the Problem/The Lesion
It is important to attempt to find where the problem exists. The problem may lie in the CNS itself with decreased perfusion or
can lie in the lungs (decrease exchange of gases), circulatory system (decreased exchange of metabolites), local tissues, local
nerves, etc. So sometimes, a CNS presentation is not a CNS problem because other systems may manifest problems into the
CNS showing ―neurological signs and symptoms.‖
Ex…A GI polyp that causes tinnitus…There is occult bleeding from the rectum. Blood loss creates anemia Anemia leads to
lack of oxygen delivery to tissues (hypoxia). Hypoxia affects the CNS via decreased oxidative phosphorylation and ATP
production (energy levels or ATP levels drop). The hypoxic state affects the brain manifesting as increase in CNS function and
Breakdown of Blood Flow through the Carotids and VB System
60% of blood to the brain flows through the carotids. 40% of blood to the brain flows through the VB system. The exception
is the post. cerebral artery that gets flow from the VB system.
VB system and stroke
10% have absent or vestigial VB artery. In these patients with an absent VB artery, the other artery is usually much
larger to compensate. As lumens narrow in large and medium sized vessels, small vessels open up to compensate. Brainstem
functions can be impacted by changes to VB flow. Signs and symptoms of VB insult are the D’s and N’s.
Dizziness: The vestibular cochlear nerve
Dysphagia: Trigeminal, Hypoglossal
The three above are in the pontomedullary area
Diplopia: Abducens (#6)…Motor control for eyes with eyes shifting in different directions
Ataxia: Wide based gait…Watch people walk. People should walk with symmetric gait. Walking is falling and catching
oneself. We keep our feet normal in regular gait. If balance fails, the base becomes wider and wider. Ataxic gait is broad
based and waddling. The cerebellum can’t process the input. If the brain can’t combine the information, we broaden our base.
Little kids walk with arms out to balance, and over time the pathways refine and the motor program for gait is stored in the BG.
Nystagmus: Connection between 8, 3, 4, 6
Nausea: Area pro-streama: Responsible for vomiting, with no blood brain barrier, picks up toxins in the system
Numbness: Long tracts that run through brain column
*** Syllabus and Web based assignment for stroke ***
Vascular Problems and History
Past medical history, family history, medications, social history all should be checked. In the past medical history, issues like
cholesterol problems, blood pressure problems, cardiac problems (history of prior heart attacks), prior history of TIA’s,
walking distances and legs cramp (vascular problems – usually systemic problems), medications (aspirin a day, warfarin,
platelet inhibitors, etc) should all be taken. History is a tip off. The D’s, A’s, and N’s (listed above) are of particular
Ex. Dizziness…When a patient complains of dizziness, you have to qualify in 1 of 3 systems: vertigo (problems with
vestibular apparatus), dizziness (unsteady on your feet – proprioceptive problem or sensory input problem), or light
headedness (cardiovascular system). For example, if the presentation is ―the room is spinning‖, it indicates a vertigo issue
from the semicircular canals and labyrinthine area.
The test is worthless. When you auscultate over the carotids, you listen for bruit. If you hear a bruit, it doesn’t mean that the
carotids have a bruit, but a problem exists somewhere in the system causing pressure changes that can be felt/ausculatated at
the carotids. The problem can be at the heart, kidney, lungs, etc. You still have to listen to the heart and screen other areas to
determine the source of the problem.
Impact of a Murmur & BP
A murmur in the aortic valve is transmitted up the vascular tree to the subclavian and carotids. The aortic valve murmur may
calcify and the response is shoving blood up the tree towards the brain. Aortic valve stenosis causes the amount of blood
passing through during contraction to decrease. If the amount of blood decreases, the amount of pressure at the carotid body
decreases. The body needs a certain pressure to perfuse organs and undergoes pathological changes if the amount of blood or
pressure of blood is not adequate. If the carotid body senses decreased pressure, the response will be to increase contractile
strength in heart causing increased blood pressure. (via vasoconstriction), increased HR, and increased respiratory rate.
We have baroreceptors in the aortic arch that help to regulate BP. The kidney also assists in BBP via the JG apparatus and the
rennin-angiotensinogen-angiotensin mechanism. BP goes up to perfuse tissues when the mechanism is triggered. BP is not a
problem, but the atheromatous plaque somewhere in the system is the problem. The test causes the sound of the bruit, that
may/may not be heard at the site of the plaque. The sound could be heard proximally or distally. In the case of George’s test,
the sound heard at the carotid could be the result of a problem elsewhere.
Motor programs are stored in the BG. If we have problems, with perfusion of MCA (middle cerebral artery) we have BG
problems. Circulation changes with the MCA causes motor system failure. We can see problems of the sub-thalamic
nucleus and we can have hemi-ballistic activity.
If we don’t get blood to tissues, neurons break down and destroy other neighboring neurons.
The MCA is a branch of internal carotid. If the MCA is occluded by a plaque located at the internal carotid
bifurcation, the result can be problems at the posterior limb of the internal capsule. The internal capsule will show a
hemi-paretic stroke (a stroke of the post. Limb of the internal capsule)
Internal Capsule vs. Cortex
Problems of the internal capsule will show as widespread problems due to the anatomy of the capsule as fibers from
various pathways all converge/pass through this area. Cortical problems usually show up as isolated/specific location
problems as the fibers diverge to specific locations of the brain.
Aneurysms of Vessels in the Cranial Vault
Tunica media may be missing at the bifurcations along the ant. comunicating artery of the circle of Willis (present in 25-30%)
and at the post. comunicating artery of the circle of Willis (present in 20-30%). The tunica media is missing because of the
location at the bifurcation zone and function (presence of the media causes contraction…so you don’t want to have contraction
at a bifurcation zone because it can shut two vessels down).
4 Types of Headaches
4 primary headaches types: migraine, tension, cluster, chronic daily
The incidence of inter-cranial aneurysm is 5-7%. There is a headache that goes with it. The location of the headache is
consistent at the same location all the time. The aneurysm doesn’t move. The headache is pulsatile because the aneurysm
dilates with every pulse. It is of variable intensity depending on BP, stress levels, and other triggers. You can have the
aneurysms and not have the headache, depending on situational factors.
Upper cervical cord and thoracic cord = Are perfused by the vertebral arteries.
Thoracic Cord = Radicular branches perfuse down to the mid thoracics.
Lumbar Cord = Artery of Adamkiewicz perfuses the lumbar cord (the artery is a big branch responsible for the L/S plexus).
Information goes to the cingular cortex (located adjacent to the Corpus Callosum). The cingular cortex fires to the association
cortexes for storage. This is the pathway for memory and part of the limbic lobe. Damage to the ant. spinal artery and cingular
gyrus shows as problems with recall and memory. It also feeds the orbito-frontal cortex for excecutive function.
1). Cingular Cortex (limbic lobe…fires to the association cortex)
2). Association Cortex (storage)
Falx Cerebri and Meningiomas
In between the two hemispheres is the falx cerebri. Tumors affecting meninges are called meningiomas.
Meningiomas can impact both lower extremities vs. Damage to the ant. spinal artery may affect only 1 LE.
Chorea, athetosis, dystonia, tics, tremors are examples of dys-kinetic activities. These are movements when you don’t want it.
Dys-kinetic movements are caused by disinhibitory syndromes. The GP interna tonically inhibits the thalamus (holding it in
check). The thalamus gets all sensory and motor and serves as a distribution center, taking in information and sending it out.
The BG holds the thalamus in check keeping motor movement in check. Shutting down the inhibition activates the cortex and
causes unwanted motor movements.
Parkinson’s is disinhibition (therefore facilitation). Choreiform movements, athetosis, tics and resting tremors are
performed as a result of lack of inhibition. These movements are resting tremors.
Activating the whole pathway will shut down the tremor in early states of the disease. Often, in late stages, there is nothing
that can be done as dose tolerance is achieved (with medication). Doctors pull them off the meds and cycle them in and out to
decrease unwanted movement.
Location of the Internal Capsule
Between thalamus and BG. The MCA (middle cerebral artery) affects the internal capsule.
Voluntary motor pathways for head and neck
Of the intracranial bleeds, venous is better to have than an artery bleed. In the arterial side, the pressure is higher as the
arterial system is a higher pressure system moving more blood into the vault. The arterial system takes up more space and
causes greater brain motion, moving the brain down and across the FM. Tthe brainstem squeezes down the FM. The medulla
and pons are squeezed and the vital center shuts down. The brain tries to save itself by increasing BP due to increased volume.
Pulse and HR slow during the epidural hematoma.
Lucid interval: Patients may experience lucid interval with intracranial bleeds. They need to be monitored constantly as they
can crash. These patients go through periods of appearing fine and then crashing due to the pressure within the cranial vault
and the impact on the vital center.
Cushing’s = Increase in BP, slowing of Pulse and decrease HR
Bleeding into the Vault
The brain can shift in 5 directions.
1). Uncal Herniation: The most important shift is the uncal herniation. In this shift, the uncal processes of the
brain herniated through the tentorium cerebelli. The highest cranial nerve in this area is CN #3. #3 is motor to the
eye (extra-occular) and visceral motor control (parasympthatics controlling pupillary size). Uncal herniations first
affect CN#3 changing conduction of the nerve. The pupil dilates because it is unopposed.
2). Subfalcine Herniation: Cingulate gyrus shoved under the Falx Cerebri. Memory is OK because the ventral and
caudal components of the cingulate gyrus is where the information crosses.
3). Tonsillar Herniation through FM: This is Arnold Chiari malformation. Type 1 in congenital. Type 2 is after
4). Sub-tentorial Bleed: Herniation up through the tentorium. This situation doesn’t happen very often.
The brain sloshes around with trauma and you worry about swelling. Cognitive decline, brain swelling, mood alteration, and
increased intracranial pressure may be present.
NEUROLOGY – 6/5/08
LOCALIZING THE LESION
Ex…Patient presents with : Weakness in the right lower extremity of a couple weeks duration, with no notice of sensory
changes, no tingling or numbness, but when they put their foot down it gives/bounces a little bit…Where is the problem?
Once you take the history you take diagnostic approaches to where the problem is. In the history process you are not just
gathering information towards a diagnosis, but you begin the process of memory and recall. As you get older, you have to link
things to other important events, so history can actually check cortically driven processes and cognition.
Is the problem motor or sensory? It is a motor because of weakness. Is the weakness flaccid or spastic?…Flaccid makes it a
final common pathway and if the weakness is spastic it is an upper motor neuron (from cortex to the lower motor neuron in the
anterior horn cell). If the problem is in the UMN, you must determine where the lesion is so that diagnostic images (MRI’s,
etc) can identify where to take the pictures at. UMN could be cord (C-spine cord, T-spine cord, L-spine cord, Brain, etc.).
*** Laminate the chart and use the chart as Cliff notes ***
Where the problem is? Cortical Problem, Subcortical Problem (basal ganglia and thalamus – reside in the middle of the brain,
thalamus adjacent to third and 4th ventricles wwith BG lateral to that with internal capsule in the middle), Cerebellum (perfused
by the vertebral basilar artery), spinal cord (outside of the cranial vault), LMN, plexus, named nerve, NM junction, Muscel
You have to assess the whole pathway from muscle all the way back to brain. Muscular dystrophy is a myopathic process and
genertically inherited This refers back to the muscle.
Cortex – Funciton: Intellectual capacity and cognitive abitiles, the home of sensory ability and motor initiation (precoritical
spinal pathway and corticospinal pathway)…A problem in the cortex in the insula or occipital area or post central gyrys (we’ll
see changes in the sensory experieces…Occipital pole = vision problems…Insula = audisotry stimulation….)…Motor system
and cortex (movement…the motor system starts with the initiation to move then BG, Thalamus, etc….temporal lobe
dysfunction and we may have problems initiating movement)…Hyperactivtiy of motor cortex could be created by epilepsy
(Dilantin is a neuroleptic or antiseizure medication)…Seizures do not equal epilepsy…If you have overactivity with spiked
waves of motor cortex, you can gerneate epilepsy…Seizures are cortical activity due to another bodily issue (hypo or
hyperglycemia, Calcium irregularities) that causes the corticospinal pathway excitation and the ultimate result of a seizure…
Sticking a needle in the arm…Where is the problem? Receptior, Named Nerve, Pathway, Cortex, etc….That is why you have
to do all the pathway checking.
A mass in the brain (meningionma comrssese tissue and deals with vascular tomcpression)…Intially you’ll feel tingling and
then ischemically it shuts down. The loss of sensation could be cortical phenomenon or anywhere along the pathway.
A loss of motor function from the top will cause spastic problems. Cortex disconnected and you go spastic. They’ll be reflex
changes, pathologic changes, etc.
Sensory changes and you wont’ see motor changes. You’ll only see loss of senation.
Cognitiion and Intellecutal capabilities…Stephen Hawking (his body doesn’t work but his brain does)…Cognisitive declines
think about cortical impact. You’ll see this in dementia, Alzheimers, etc. Levels of the cortex don’t function properly. Testing
cortical capacity can be acheeived by memory or testing mathematical testing. Start at 253 and subtract by 7. That is way to
test intellectual processes and cognitive abilities.
In athlete concussion, you actually test the RAS (reticular activating system) which in turn affects the brains ability to perform
cognitive function. You’ll do the same test of subtracting by 7, but the test is for a slightly different function.
BG and Thalamus…BG stores the motor program. D1 and D1 pathways and dopamine receptors. A breakdon in the pathway
is called disinhibition. Breasking down the inhibition loop, we know lose inbition from the GP interna and activate the VA
nucleus of the thalamus, which affects the cortex and causes movement. We don’t want to move (think parkinosn’) they can’t
stop it unless, they want to move it. The movement goes from movement at reast to nice smooth movement (early on). Later
in the diseae they shake all the time. BG ives us tremors, ticsk, myoclonus, atonia, athetesias (?). Myoclonus is movement in
acouple direction with a jerk. Movement when you don’t want any is a function of the BG. Changes in muscle tone occurs
with BG. Parknsons, they get rigidity not spasticity. Parkinsons (tremor, ridigty, akinesia, )…Parkinsons gait is breadiend and
shuffeled (muscles so tight, they don’t move well)>
Thalamus damage: You lose primary sensoty expireioenex (pin prick, hot, cold, touch). They don’t have any sensations
primary. Priamry exeprieences are necessary to activate the cortex, to get a second sensory experioece to recognize what is
going on. Ex. Putting a safety pin in the hand (and they won’t recognize it because the thalamus is lost and won’t transmit to
Cerebellum: Modulates motor activity to the satisfaction of the cortex. Ex. Picking up the glass of water and you;ll shake
trying to modulate the activity for a smooth movement. Cerebellum is inbibitory to the cortex. The cortex tells the
creelmeullm it wants to move and the cerebellum can’t coordinate and you get the end range intention tremor. It tells where
the lesion is. You may also see disdiadokinetic activity. Rapid hands and palms movement on the legs. Touch the finers
together with the eyes close, or run heels up shin. Cerebellar ataxia and gait gets broader.Normally the legs should be 2-3
inches and no more wider. People on antiseizure mediation will be broad based gait (because you shut down).
Rebound Phenomena: Holmes Rebound….Cerebellyar disease and you activate your muscles and you releae them and see
what happens. Patietns with crebellar dieseae can’t stop their arm or leg and it keeps moving. Holmes rebound phenomena the
patient can’t predict end stage and they can’t stop the movement.
Headaches: Do a cranial nerve exam…Things causing head pain (intracranial aneurysm…changes in pressure from
hydrocephalus, tumor, etc.) A common link may be the creanial nerve exam. You won’t find much (maybe 1% of headaches
may show cranial nerve deficits), but it is possible to find the problem and possibly spare the life of 1 patient. An intracranial
tumor is significant. If you find 1 intracranial mass,, and you help them by doing the cranial nerve assessement or knowing
what metastasizes to the brain, you can help the patient. Melanoma loves the brain (it takes 1 cell to cause malignancy in the
brain). If you take 99% of the tumor out, they leave some in there. IF they even can kill 99% of whats’ left, something is left
and that is all you need, like the tumor will come back.
You have to look at cranial nerves…Since the cranial nerves come from the brainstem, you evaluate the space btwenn the brain
and the spinal cord. Motor pathways run through there, autonomic pathways run through there, sensory pathways runt hrough
that space, so all seosnroy and motor goes through the rbain stem along with cranial nerves. CN 1 and 2 are direct extensions
of brain (you don’t evaluate brain stem per say).. PUpillary reflexes can deal with visual input so sometimes you use the eye
innvervated by 2 as a window to look thoruth. 3 and 4 off the midbrain. 5-8 come out of the pons as a general rule. 9-12 come
out of the medulla as a genral rule. The caveats is that the 5 th cranial nerve has many nuclei in different locations. CN 11
comes off C1, C2, C3, C4, C5. The component off the medulla is an acceosssory component to the spinal nerves and hendce
it’s name. There is a comcponent of 11 that becomes part of the vagus and a component that affects SCM and trap.
CN 3, 4, 6 affect the eyes and you look in the midbrain and ponse.
Hearing and balnce with hoarseness, look at the medulla and pons. The 8 th nerve sits between the meduall and pons.
All the spinal pathwasy and cranial pathways to get to the cord, pass through the brainstem. Long track signs…The 3
pathways we can assess with accuracy dorsal column, lateral corticospinal, lateral spinothalamic with regards to neural
Check refelexes, sensory experience and motor….If all three present check the brainstem????
Can you have isolated enrve lesions without long tract signs? Yes, Bell’s Palsy, Tic de la Rue, Anisocoria (CN 3 lesion)
Long track signs are a deficiency in one of the 3 above pathway (dorsal columns vibraition or light touch that is not part
of a particcluar dermatome – that means you affect the dermatome)…Motor problems with long tract signs (are UMN
lesions that show spastic paresis, clonus, etc.)
Abdomnal Reflex: Bad reflex to test…
You can’t rely on dermatomes in the upper extremity? There are so many charts out there that show different dermatomes.
Long track signs are vague not very descriptive problems.
Does it matter if the lesion is from outside in or inside out? Yes, because of how the cord is somatotopically organized.
Loos of pain and temp in LE at L2 nerve root. IN 2 segments it crosses and ascends up the cord. You have a laminar
distribution in the cord with theinformation more peripheral. Extraduarl coming (from outside squeezing in), youi;ll see
ascending loss of sensory perception. If the problem is down low, it won’t affect the C-spine. If it is up high, it affects the
Upper and lower extremity.
Motor is the same way. C-spine comes down and wants to be closer to the ventral horn. LE will be more lateral in a laminar
distribution. Outsdie squeezing in will affect LE first.
UMN signs, and a well demarcated sensory loss….Ex. a T6 right side of cord problem and you;ll lose pain and temp
(spinothalamic) on T7 and T8 and below on the other side of the lesion (left). You can lose ipsilateral Dorsal column on the
right side (vibration, deep pressure 2 piont)…This helps tell you where the lesion is. The lesion has to be big to affect bpoth
tracts and both sides. The corticospinal pathway can also be affected with ipsilateral changes of the UMN variety. Are
compressing the cord or the vessels? Now it changes, because we have collaterization..Ant. spinal gets ant. 2/3 of the cord and
post. Spinal ….. Ventral root and we can see segmental motor changes and if the dorsal root is involved, we now get anesthesia
at that level.
Dermatomal Distribution of sensory change: Specific to geographic area and more reliable lower extremity. Dermatomoal
sensory loss and mytomal motor loss and reflexes related to segmental level. The muscle tested for L4 nerve root (tib ant. –
strongest dorsiflexor and slight inverted)...
Look for fasciculations…When you get an increased in pressures…you get a change in the sodium potassium pump…You get
influx of calcium and you’ll get acetylcholine in the snapes with spotantoue firing of the muscle…That is the mmotro’s system
response that is analogous to the paresthesia of the sensory system. Fialure of the mitorchondria to oxdiae, failure of pump,
leakeage of elctrolytes, cause of potentials and fasciculations. As you get older, the disc dimension thins and the vertical
dimension of the IVF deceases. The AP dimension decreases. Over time the pressure in the compartment increases. We are
OK till central canal stenosis. The abrupt changes occur first.
NM disease...there are no changes in the sensory system as we fail to fire the muscle. We either get an autoimmune reaction of
post synaptic derminus that faisl to recognize acetylcholine or we fail to produde dqequat eacetlcholine. The mauscle does not
fail all at once. Over the course of time (ex. A full daY) as the day wears on they get weaker and weaker. When we examine
them n the morning,they are normal. So our conclusion is skewed….WE then look for an interval changes (weight change).
The reasonable provider then acts the patient to stop by later in the day. We notice muscle weakness. The muscle that works
almost the entire period of the day is the eylids (levator palpebrae superioris). It is a little muscle with great fatiguability. It
takes less to wear down. We examine the patient, to sustain upward gaze for 30-60 seconds. The muscle is innervated by
CN#3. Superior rectus by CN#3…so when you look up, they both have to work. IF te muscle fials from NM, disease, the lid
will drop like a curtain. Then you identify the diseae and can properly determine course of care (possible refereral to a
specialist for medications).
This is an autoosmal recessive trait. Check the family for similar problems.
A hint is to determine who lives there (normal anatomy) and who visits there (what pathologic process can reside there)…The
chart will help guide you to strategy…
Intracranial masses weaken vessels. As the tumor grows, the peripheral vascular system changes. Tumors can create
angiognerses. It sucks new vessles in to feed the tumor. The vessels are not of the same quality and can rupture and cause
hemorrhage. They patient can suffer from the hemorrhage.
A middle aged woman appeared in the clinc because of difficulties in wlaking a saggin of her mouth. Her history showed that
these abvonlalties were the lates in a long series of events. About 5 years prveiowly, the woman hasd a series of dizzy spells
and complained of tinnitus in her right ear. SErveral years, later, the noised didaspperand and she noticed a hearing loss in the
same ear. Somtime later, she found it diffucult to lcose her right eye tightly and the corner of her mougth on the right began to
droop and di not rise when she smile. Recently, she began to exeriprecne itntermitten painful sensation in the right side of her
face and now it has become bumb. Within the past fes weeks, she notices a tendy to sway to the right and while walking she
often staggered an somtiemes fell to the right. The se most recent evetns bhave been accompanied by difficulty in swallowing
and hoarsemness. In addition to the above, nerulolgica exam also revelaed a loss of taste on the right side of here t ongue, No
corneal reflex coujld be elicited from the right eye.
1. Specify each individuaol abnormality identigied and mane the neurologic structure or structures involved (nucleaus,
cranial, nerve, peripheral nerve, neuroanatomic structure).
2. List the possible diffenetial diagnossies by system (VICTANE).
3. Locate the site of the lesion.
NEUROLOGY – 6/12/08
By 2010, 17% of the GDP will be spent on health care. WE don’t rank in the top 5 in the world in health. Our system is
clearly not working.
What does the adjustement do?
Increases mechanoreception that decreases nociception. This decreases stress hormones in the body. Ex. Lowering the cortisol
reduces the autonomic response and decreases the . The adjustment is similar to exercise. The therapeutic benefits of exercise
is increased caloric burn (effect global BMI), improves glucose metabolism, decreases LDL and lowers total cholesterol,
increases serotonin pathways (mood, sleep and affects depression), drops blood pressure (decreases catecholamines), moves
white cells better (to expose them to more pathogens).
Nocicpetion is perceived with stress. Stress changes hormonal levels, use of building blocks amterials, production of
catecholamines, etc….Nociception and stress is a mechanism that is well linked with poor health. If we can link, the
adjustment’s affects with some of the relief associated with exercise, we can have some overwhelming evidence.
Do you need to take insurance?
Yes, to get started and get patients in the door, that may otherwise have no access to you…No, later on after several years and a
steady patient base, you may not want to take insurance. You can opt of the programs later in time, by giving the patient and
insurance company 6 months. If the patients trust you and you have a good reputation, you should be fine. The copays are
traditionally $20-40 per month. If you charge them $45 per visit without taking the insurance then you should be OK.
Medicare reimburses for about $30 per visit. If we go to national health care, they may use the Medicare model. You’ll need
to repay your loan $1,500.
Dizziness means unsteadiness. If the room is spinning that is vertigo. You have to get clarity as a practicioner. Vertigo
(semicircular cancals attached to Vetsitbular part of 8, that goes into pontomedullary junction, collarterzliaing to the
cerebellum….secondary system goes to vestibular nucleus). She’s had the condition for 5 years. The tinnitus is followed by
deafness (killed the 8th cranial nerve). The nervous system first response to hypoxia is to increase (tinnitus, dizziness) and then
later destruction (deafness – shut down). You go from 55/100 mL of blood to 25/100 mL of blood to 12/100 mL of blood and
the system goes out altogether (deafness).
Lesions of the cerebellum we fall towards. The peduncles (superior, inferior, middle). Superior peducnlce info leaves and
goes to cerebrum. Inferior to cerebellum from periphery. Middle from cerebrum and into cerebellum. The middle part is
attached to ponse and the inferior is attached to the medulla. So, we think that pons/middle peducncel may be affected. With
a cerebellum lesion, they fall to the side of lesion. The patient falls to the right, right sides lesion.
R cerebellar lesions n the ponotmedullary juctnion is what we think
Difficulty swallowing -- #10 (Nucleus ambiguous)…recurrent laryngeal nerve (treponema pallidum can affect #10 and cause
On exam, say ah…we will see an uvular deviation with failure to elevate on the right, so the uvula deviates to the opposite side
of the lesion.
Loss of taste…7 and 9….Based on preceding exam findins, 7 is already involved, 9 is involved, and so is 10.
Corneal reflex...Absent, nothing blinkes on the right and on the left they blink…
Tottal 5, 7, 8, 9 & 10 (right)…Where is the lesion? Go back to the chart (in the brainstem we have cranial nerve + long tract
signs = brainstem…but it not a brainstem lesisn because there are no long tract signs, so it is outside the cord…That is how we
can find out it is an acoustic Neuroma).
As the lesion expands, it smashes outher structures. The lesion didn’t damage the other structures. We look now at the
ischemic penumbra. We don’t perfuse, we become hypoxic and shut down metabolic processes and the system doesn’t work
well. The system is not dead yet. Over time if the lesion would exapnad to the cord, we would eventually signs and symptoms
of long tract involvement, but right now it is only a cranial nerve issue.
Glutamate cytotoxic Cascade
As we start down the hypoxic/ischemic penumbra…The cascade can occur. When neural structures are compressed by
smoething (ex. Herniated disc)…Tissue is not dead yet, and is still alive but not functional (55-30ml/100). The numbenes and
tingleing goes away and you have anesthesia (15 ml/100). Once we get below the ioselectric point, we cannot maintain. We
have not lost the entire dermatome, but we have lost part of the dermatome. We see a conduction block. We need energy to
keep the cell alive and from dying. We need ATP (phosphate bone to create energy). We are not getting this from the
mitochondran via oxidateive phsyorpheraltion. The membrane is phospholipi.d We tera down the membrane to now create the
energy. One of the byproducts is the release of phospholipase the breaks the membrane down and the byproducts are
arachidonic acid. We are now intoth e arachindiconic cascade under cycooxeganse pathway Cyclooxygnease causes
generation of prottaglandins and lipoxogyngase creates prostaglandins. This creates local infmallmatins and causes swelling.
Swelling ampligies the ischemia and causes the system to work even less. The cell dies from nectrotic liipofaction. When it
dies, the cells walls don’t function. A dead body and clells liquefies. It turns into thliquic as the cell dies and releases
constintuies into the adjacent tissue. They are hyposmolar and bring in more fluids, wchi menas they drive in more electolytes,
fluids and cause further swelling of adjacent tisues, leading to more inflmamtion and cell wall problems and death of adjacent
tissues. You lose pieces at a time. You treat people with neuropathies and you can help with pain. Tehre may be people with
some small areas of neuropathy, because the tissue has died. The dead tissue won’t return function. Yonger patients will
recover better, because theyir physiological reserve is better vs. older people whose reserve is lost.
We lose parts of the nerve. Can wer recover the entire nerve if we get it soon enough? Yes!
Cauda Equinae Syndrome – If we get there soon enough we can spare neurologic function, and if we get it late we don’t
Clost busters: Used after stroke and heart attack…We need to use within 3 hours. Within 3 hours, if we have a clot that has
caused a problem in the CNS, the same process occurs in the capillary beds. Cailllaery endotehieulm gets the blood and
nutrients from the capillary. Blocking the capillary if the tissue continues to pull O2 and gets CO2 stores, it becomes more
acidic . pH changes causes dilatrion to try to get acidity out. It brings more blood and furthers the process of CO2. The
caiplllary undergoes the above cascade to eventually pull the phospholipid membrance apart and cause destruction. A clot
bluster turns an ischemic event into a hemorrhagic event, we go from dry stroke to bloody stroke. All because of a series of
evetns that breaks down tissue. This is all due to lack of O2 that affects oxidative phosphorylatin that creates subsequent
*** Know the chart…If you can understand how 1 cell works, put that into the tissues, orgrans, organ system works ***
Hemoglobin bnds to perforin ring. It is in the red blood cell. Defictis in the ring creates motor weakenss as we can’t deliver
O2 into the tissues.
MOTOR DEFICINTS (CH 5)
The cause of weakness is best determined afte the disorder has been localized to particular reion of the the neuromuscular
system by any associated signs and symptoms.
Ex..Sensory problem of dorsum of foot along with Extensor Hallucis weakness….Assoociarted SNS of L5 nerve root lesion
would be Sings and symptoms (back hurts, pointing to the low back, can’t feel foot, can’t raise big toe).
Hereditary causes of weakness must be excluded, if necessary by examination of other family members. A number of
hereditary disorders have variable clinical expressions can dan be identified by genetic testing.
The distribution of weakness is helpful in distinguishing between a radiculopathy, plexopathy, and peripheral neuropathy, and
between neurogenic and muscular disorders.
If it doesn’t fit in radicular, named nerve you will be in the plexus. Plexopatheis are complicated.
Autonomous zone….Ex.Radial nerve innervation (3.5 fingers)…Ex. Median Nerve (1.5 figers)…A radial nerve lesin will show
eakenss extending wrist and elbow, so you check the autonomous zones side by side. There may be a deficit there. This also
explains tricpes and wrist extensor weakness and brachioradialis reflex.
Wakness that is patchy, varies in servertiy with activity, and does nto conform in distribution to the terroty of a nerve or nefve
root sugest a disorder of neuromuscular transmission. (The most sensitive way to test for NMS junction problem is to have
them look up, the levator palpebrae superioris fatigues quickly).
It is important to be aware fo all medications that have been takens as motor disorders a telvesl of the neuromuscular system
may be drug related.
Ex. Look at the smallest muscles you can to test. If takes less force to work the area. The small muscle groups are typically
Motor function can be impaired by lesions either centrally or peripherally
Control of motor activity involves several parts of the nervous system
Medullar decuassatoin of pyramidal tract
Post _ Limb of internal capsule
Hemiparetic stroke = loss of inbition to nuscles above t6 (flexor postureing) and losss of inbhition to posterior muscles below
t6 (extensor posture)…They swing a step leg around (knee exteneded, hip extended, and foot plantare flex)
Corticobulbar pathway = gives motor deficits in the cranial nerve (speech, sqllowin, facial drooping,)..btw. thalamus and BG
Motor fibers of the peripheral system have their origin in th elwoer motor neurons
Lesions at any level of the in the PNS can disturb mtor function as can myopathies
Anterior horn cell
Weakness, Heaviness, Stiffness, Clumisnes,, Incoordination, Difficulty excuting movements
NEUROLOGY – 6/26/08
*** Test will cover the where is the lesion sheet. Questions will not be from the sheet per say, but a case scenario based on the
information on the sheet of where to find the lesion. The information is given from you. You have to identify, recognize,
integrate, and find where the lesion is. ½ the exam is fill in the blank or short answer. The fill in the blank portion gives you
some wiggle room if you get the concept. You have a better chance to up your grade if you understand the concept. ***
*** The motor system powerpoint has already been uploaded. ***
*** Know pgs. 233-244 in CH 7 of the textbook ***
*** Test will be 50 questions with 25 being multiple choice and 25 fill in the blank (subject to change) ***
*** Be familiar with the ischemic penubra 55ml per minute…If we get down to a bout26-30 we see EEg changes. At 12-15
we see isoelectricity. At 6-8 the nerve is dead. ***
*** Know the flow gradient. Highest in the artery and lowest in the veins and venules. If there isa change we head dowhn the
venous staiss process and we haed into anerobic glycolytic process and fail to make ATP due to laci of glucose and oxygen and
as a result pumps fail. This havppends in nere and muscles. Taking calcium off troponin won’t occur and it will cramp in
muscles and the process shuts down. ***
*** Blood Supply – Know the anatomy and blood supply to the anatomy. Understand what part of the brain is persufed by
what vessel. Post. Apstct of heimispher – Post. Cererbarl…Above the Tent…Below the Tent ****
*** Cranial Nerve Locations are somewhere in that scheme. ***
*** Stroke course will have included information. ***
*** Know the consequence of VB flow disruption. 5D’s And 3N’s *** (Dysphagia, dysarthria, etc….nystagmus, nausea, etc.)
*** Flow Gradient… PA greater than PC greater than pf greater than pV greater than pT…Disc, facet hypertrophy,
osteophytes, involvding of ligamentum flavum all can make the IVF smaller. In the IVF, we ave nerve arteries and venous
system. The lowerst pressure system succumbs first. Pressures on the vein and return (venous) slows. If it slows too much,
the IVF becomes more narrow and blood is pumped back to the funiculus. The nerve root is a bunch of bundles and around the
periphery we have the big part we have the perineurium. The perineurium warps the nerve together. There is some elastic
tissue in there. We have a collagen amtriax with some elastic tissue. The enrve swells to try to relieve pressure on the vessel.
Once we pass the tolerance, we back blood up into the capillary beds and that slows the exchange of gases and metabolic
producs. We go into infomamtory process and drives up the pressrure that promotes less exchange. Inflammaotry porceses are
more metablliclly active processes and we burn up the metabilities quicker. The capillary can no longer exchngaer and we go
into a hypoxic state withint the nerve. We can’t phosphorylate making ADP to ATP. The pumps will fail and ther nere is
hypeexcitable with numbness and tingling. The nuerve will become numb eventually (isoeletcris). We have ciapilliary stais
leading to arterial statis (blood doesn’t move through anymore). The nerve fiver to last succumb and to adapt is C fobers.
What remains is everyting is gone except pain. That pain becomes central pain, chronic pain. ***
*** The presurer in the artery is greater than the capillary. Capillary is greater than the funiculus has to be greater than venous
pressure. The pressure in the vein is greater than the tunnel.----When we talk tunnel we talk mysofascial, bony or a
combination (ex. Carpal Tunnel, Thoracic Outlet tunnel, etc).. Pepople who wait too long for carpal tunnel surgery injure their
capillary beds long term. The long term damage injuries the ability of the tissue. Phosopholipase and arachindonic acic.
Cycol and Lipooxygenase are activated. Proinflammagltyr constitutesnt are relased that. A comprosed cell wall tries to
contain more stuff….An analogy is a levee. The levee is breaking down because it can’t handle more pressure. As bpressure
builds, the cell wall explodes. Eventually there is a fibroblastic infiltration, and scar in the nerve. The nerve scars. CT patients
if untreated and the condition reimains with anesthesia, because the nerve is dead. The nerve can’t conduct a potential and the
nerve dies. Sensation is gone. WE do save the important stuff like unconscious proprioception but we lose things like
*** Icing slows the metabolic breakdown. It slows the infallamtroy process. Swelling can compress the cord during Spne
injury. During a concussion swelling a tht brain level, leads down the ischemic penumbra ***
*** The ischemis penumbra is based on everything normal. The heart is a good pump (heart defects alter the pump ability –
ex. Mitral stenosis, Status post MI). If you don’t perfus the tissue adequately the pulse goes up. In a physical exam is ccalled a
vital. We have to have the right type, location and distribution of cells and the right hempatoipics. In anemia, we have to pump
more blood so the rate incrases. Respiratory rate has to increase (lung disease – same problem). ***
*** If you are hypoxic from COPD and a heart pump, are you nutritionally gonna fix the situation. ***
Disorders of Somatic Sensation
Joint Position Sense
2 point Discrimination
Sensation from the soma ―body.‖
Abnormal Spontaneous Senations (Burining, Tingling, Pins and Needles)
Unpleasant sensation generated by innocuous stimulus
Sense of heaviness, weakness, or deadness
Paresthesia is spontaneous sensations. That is the pins and needles
Dysethesis ais a precursos to allodynia. Dysethesiaiss a perverted sense of sitmulation.
Numbness can be linked to some motor problems (heavy or weak)
Complete los of touch sensation
Partial loss of touch sensations
Increased sensititvity tou touch sensations
Sensation should be symmetrical. You have to check one vs. the other.
Complete loss of pain
Partial loss of pain
Hypealgesia or hyperpathia
Increased sensitivity to pain
Compressing a nerve root and you lose large diamtere fibers frrst but have normal pain.
Misperception of a trivial tactile sensation as pain (RSDS & CRPS)
More common to females. Ex. After a fracture the entire extremity becomes painful. Neruons take mechanical stimulatin and
transmit them as pain. This is a central process.
After a trivial injury, over time the pain becomes intolerable. RSDS and CRPS include an autonomic component. Nociecption
fires into the autonomics and RExed Lamina’es including the autonomics in the cord. Therie is a sympathietic component.
They used to remove the sympathetic chain. In the UE, they used to anesthetize the sympathetic cahin canglion.
If a person loses pain and temp and everything else is intact, Syringomyelia (symmetric distribution of loss of pain and temp
usually due to a cavity forming in the central canal).
Unilateral loss of pain and temp – could be interior or exterior to the cord. Compression of the patheay could be due to PLL
hypertrophy, stenosis, compression fracture with retrpulsed fragemetns. The pathway is vulnerable. Bony integrity is not as
Extrameduulary mass compressing the cord from the front, you can lose pain and temp in ascending fashion.
Compressing from the outsite we smash, leg, first and then going up the cord. We have to look for the level of compression.
Compression frm the back affects doral columns first.
If we compress from the anterior first, we can affect the anterior spinal artery (lose pain and temp, but spare dorsal column
function – hence sensory dissociation). Syringomelia can make this happen. They don’t feel pain and temp with
Syringomyelia is usually secondary to traumatic insult. Ex. Patients in car wrecks…
Sensory symptoms are always present before sensoty signs. The patient has a subjective complaint of pain. Pateints all feel
pain at the same level. They all sit about -70 millivolts. We all respond to pain differently. We feel it but chose whter or not
to respond. We have thamolcortical progections to the sensory cortex to feel it and perceive it. The cortex then diecdes what is
important and what is not important. The cortex can say the pain is important or unimoprotant. The cortex can tell the
thalamus you don’t need some info and shut that down (and shut down the pain). Can you quantify that in the patient? We try
to use a numerical scale. You have to realize that patient has an experience before you pick it up. It just lets you know there is
somehitng abnormal going on. You have to look at the associated symptomatelogy.
Ceehck receotpr, named nerves, plexus, cord pathway, brain, thalamus, cortex – A sensory deficit can be in any one of those
areas. How do you determine where the pobrlem is then? Cortex gives you changes on the opposite side of the body and it
may not be modality specific. Thalamus problems can affect the modalities (al l primary sensory modalities – eretying is lost).
The thalamus can perceive C fiber afferentation. The thalamus is a projection center. If we lose the thalamus we lose all firing
to the cortex for that region (all priary sensory modalites0> VPL nucleus of thalamus for the body and VPM for the face. If
we have brainstem problem, we see in conjuection (nuclei of the brainstem we think long tract signs – dorsal columns, spinal
thalamic, + cranial nerves – Long tract + crnail nerve sings = Brainstem)…Cord problems (problems with sneosty pathway and
specific modaliteies with specific locations…a lesion will present specific modality at a specific site…Ex. T6 DC
lesion)…Nerve root (dermatomal and myotomal problems in a specific location)….Plexus…Named Nerve (possible toxic
expsorues, organophosphates, some medications create problems with sensoty experiences like antiseuizre meds).
Compression neuropatheis (typically we don’t deal with CNS, but we deal withperipheral problems). Mechanical Defects