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.

• 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.

2. 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.

3. 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.

4. What nerve is the efferent loop of the papillary reflex?

• Cranial Nerve 3 parasympathetic division is the efferent loop of the papillary reflex

5. Cardinal signs of gaze evaluate what cranial nerves?

• III, IV, and VI

6. 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

7. Where do the dorsal columns decussate?

• In the medulla

8. Name the three parts of the brainstem

• Pons

• Midbrain

• Medulla

9. 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 essentially- VICTANE)

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 lost- wont 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 component- innervates 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. History and physical

b. Syndromic diagnosis

c. Anatomical diagnosis

d. Etiological diagnosis

e. 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

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