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Neuroscience study guide #1
Lecture #1 9/5/14
General History and Physical Exam- Goal is to communicate!

Structure of H&P
o Chief Complaint- the patient’s age, sex, brief pertinent hx, and presenting problem
o History of Present Illness- Complete hx of current medical problem that brought the patient
to medical attention.

Includes risk factors of the current illness and a detailed description of symptoms
(chronological) and pertinent negative information
o Past medical History- prior medical and surgical problems not directly related to current
problem
o Review of Systems- head, eyes, ears, nose, throat, pulm, cardio, integumentary, cognition,
ms, GI, GU
o Family History- immediate relatives and noted familial diseases (i.e. diabetes, stroke, cancer)
o Social and Environmental Hx- occupation, family situation, travel hx, sex hx, habits.
o Medications and Allergies- all medications currently being taken
o Physical Exam- General appearance, vital signs, etc.
o Laboratory Data- dx tests (blood work, ECG, radiology)
o Assessment and Plan- begins with a one to two sentence summary that encapsulates the
main features of the diagnosis. In neuro this is separated into two parts:

Localization- based on neuroanatomical clues gained from H&P

Neurological Differential diagnosis- (arrow) more acute diagnoses are often left
at the top point of the arrow and outer edges. SEE PAGE 8 IN BOOK.
Relationship Between the General Physical Exam and the Neurological Exam

Is part of the general physical exam

the patient must be treated as a whole with problems in different systems given priority depending on
the situation

essential info about neuro diseases can be taken from all portions of the general exam
o General Appearance- how a person behaves determines mental status
o Vital signs- hypertension, bradycardia, orthostatic changes can be seen in autonomic
dysfunctions and SC injuries.

Respiratory=brainstem

Elevated temp= inflammation which could include NS
o HEENT-hydrocephalus or tumors could be congenital abnormalities.

Must be examined during TBI’s
o Neck-meningeal irritation with neck stiffness, cervical bruits with CAD
o Back and Spine- tenderness, misalignment fx, osteomyelitis
o Lymph- infections, granulomas involving NS
o Breast-breast cancer met to NS
o Lungs-diminished breath sounds with decreased movement of diaphragm could be sign of
phrenic nerve dysfunction
o Heart- embolic sources with atrial fib
o Abdomen-hepatomegaly in wilsons disease, anyeurism
o Extremities- Kernigs sign and Brudzinski’s sign for meningitis
o Pulses- PVD can masquerade Neuro disease
o Neuro exam
o Rectal- decreased sphincter tone due to SC injury
o Pelvic/Genitalia
o Derm
Lecture #2 9/6/14
Main parts of the nervous system
1. CNS- the brain and SC
2. PNS- CN and ganglia, sympathetic and parasympathetic nerves and ganglia, enteric NS
During embryological development:

The CNS arises from a sheet of ectodermal cells that fold over to form the neural tube


This tube from several swellings and out pouchings in the head that eventually develop into the brain,
while the part of the neural tube running down the back of the embryo forms the SC
The fluid filled cavities within the neural tube develop into the brain ventricles which contain CSF
Embryological development-series of 5 events
1. Neurulation: formation of the neural crest and neural tube (Brain and SC)
2. Cell proliferation: within the neural tube
3. Migration and aggregation: of cells within definitive locations (cells have specific fxns)
4. Formation of axonal and dendritic processes- communication
5. Formation of connections between the nerve cell to nerve cell or muscle cells (synaptogenesis)
Basic Macroscopic Organization of the NS
Stage 1= Neurulization
o Embryo-gastrula on Day 14 contains:

Ectoderm-entire NS is derived from embryologic ectoderm

Mesoderm

Endoderm
o Embryo (4mm)-Notochord on Day 21

mesoderm contains notochord (bundle of cells in the mesoderm)

Neural plate also develops (in neuroectoderm) and gets heavy as cells migrate
toward the center and start to develop a neural groove and crest
o Neural tube Day 28

Neural groove is continue to deepen

Neural crests begin to move closer together to each other until closes and neural
tube forms (takes one week)

Central canal is the opening in the middle

Somites are on both sides of the neural tube

Takes an additional week for the anterior neuropore and posterior neuropore to
close
o Deficits in neurulization:

Failure of posterior neuropore to close=spina bifida

Failure of anterior neuropore to close=anencephaly
The 7 secondary subdivisions of Embryological development-5 weeks
1. Telencephalon
a. cerebral hemispheres
b. cerebral cortex
c. subcortical white matter
d. basal ganglia
e. basal forebrain nuclei
2. Diencephalon-Third ventricle
a. Thalamus
b. Hypothalamus
c. Epithalamus
3. Mesencephalon-cerebral aquaduct
a. Cerebral peduncles
b. Midbrain tectum
c. Midbrain tegmentum
4. Metencephalon- fourth ventricle
a. Pons
b. cerebellum
5. Myelencephalon
a. Medulla
6. Neural Tube-central canal
a. SC
7. Neural crest
a. Peripheral nerve ganglia
2 Embryo Flexures :
1. Cephalic Flexure-brain to BS
2. Cervical Flexure- SC from BS
Stage 2=Cell Proliferation- SEE PAGE 20/615 IN NOTEPACK FOR PICTURE




Germinal layer-innermost layer-lines ventricles
Mantle layer-intermediate layer- future site for grey matter
Marginal white layer-outer layer-future site for white matter
Sulcus limitans- innermost lining that divides neural tube into basal and alar plate
o Alar plate-will be the dorsal root
o Basal plate-contains alpha motor neurons
How does the brain grow?

Myelin and Blood supply

We only have 100 billion neurons-that's it
Stage 3=Migration-know least about
1. Radial Migration-Greater distance of information from medulla to telencephalon
2. Tangential Migration-information stays at level of BS

Defects=
o Dyslexia- lack of migration
o Lessencephaly-Smooth brain
Stage 4=Cell Differentiation

Formation of axonal and dendritic processes

Development of cranial nerves
o 1st swallow and gag reflexes-14 weeks

CN V, VII, IX, XII
o
2nd visual motor system- 25 weeks

CN II, III, IV, VI
o 3rd hearing- 28 weeks

CN VIII
o 4th olfaction- 31-32 weeks

CNI
Stage 5=Synaptogenesis

Correlated with known types of permanent learning

Basis for neural plasticity

Occurs throughout development

Other parts of the brain can take over in case of injury or disease

2-20 when 2x growth of brain-----declines thereafter
Lecture #3 9/11/14
Cerebrospinal Fluid

formed by choroid plexus
o found on the floor of the lateral ventricle and top of third ventricle

circulates from the lateral ventricles to the third ventricle then leaves to the fourth ventricle to
percolate around the outside of the Brain and SC
CNS Covering-suspend brain mater to the skull

pia mater

arachnoid mater

dura mater-Falx cerebri, tentorium cerebellar
CNS organization Planes
Dorsal
Rostral
Caudal (For Cerebrum)
Ventral
Rostral
Ventral
Dorsal (for BS and Cerebellum)
Caudal
Neuron components

neurons-nerve cells

dendrites-short process receive inputs to cell

axon-carries output

glia-support cells

Multipolar- neurons having several dendrites and axons (mammals)

bipolar-neurons with single dendrite and axon (sensory vision or olfactory)

unipolar- neurons that have both axon and dendrite from a single process coming off cell body (mainly
in invertebrates)
Synapses-communication between neurons (axon of one neuron to dendrite of another)

Chemical Synapses
o
NT molecules stored in synaptic vesicles are released from presynaptic vesicles of the
neuron
o they then bind to NT receptors on the post-synaptic neuron
o this causes either an excitation (AP)or inhibition of the post-synaptic neuron
o myelin sheath-specialized glial cells (lipid)

oligodendrocytes-CNS

schwann Cells-PNS
Neurotransmitters (SEE TABLE 2.2 on pg. 20)

CNS
o glutamate-excitatory
o GABA-inhibitory

PNS- ACH

ANS- ACH and NorEpi
CNS Gray Matter& White Matter
o In CNS grey matter outside white matter inside
o In PNS grey matter inside and white matter outside
o White matter: myelinated axons (transmits the signals over greater distances)
o In PNS:

Peripheral nerves-bundles of axons
o In CNS:

Tract-DCML

Fascicle

Lemniscus-BS multiple tracts in that area

Bundle

Commissure-pathway that connects structures on the right and left sides of CNS
o Gray matter: cell bodies (Where communication occurs)
o In PNS:

Ganglia-clusters of cell bodies
o In CNS:
1. Cerebral cortex (outer portion)
2. Nuclei- BG, Thalamus, CN nuclei
Spinal cord and Peripheral Nervous System
o 12 Cranial nerves
o 31 spinal nerves
o dorsal nerve roots contain afferent sensory info to the dorsal SC
o ventral nerve roots contain efferent motor info to the ventral SC
o SC ends at L1 or L2 level
o Cauda Equina- collection of nerve roots
o Cervical enlargement- C5-T1 (brachial plexus)- thicker b/c more cell bodies (gray matter)
o Lumbosacral enlargement- L1- S4- thicker b/c more cell bodies (gray matter)
o ANS-controlled by hypothalamus and limbic system and afferent sensory from periphery
o Sympathetic
T1-L3

Thoracolumbar division

Releases NE for flight or flight response
o Parasympathetic

S2-4

Craniosacral division

ACH is released for more sedentary function
Cerebral Cortex: Basic Organization and Primary Sensory and Motor Areas
o Sulcus
o Fissure-deep sulcus
o Four major lobeso Frontal
o Parietal
o Temporal
o Occipital
o Insular cortex-in the depths of the Sylvian fissure where all lobes come together
o Longitudinal fissure-separates the two cerebral hemispheres
o Corpus callosum-connects both homologous and heterologous areas in the 2 hemispheres
****REVIEW ANATOMY PG 26-28***
Primary Sensory and Motor Areas
o Are topographically organized (Homunculus)
o Primary visual Cortex- in occipital lobe along the calcarine fissure
o Mapped in retinotopic fashion
o Primary auditory Cortex- (Heschel’s gyrus)
o Two finger life gyri that lie inside Sylvian fissure on the superior surface of each temporal
lobe
o Mapped in tonotopic fashion (cochlea)
o Primary somatosensory cortex- in post-central gyrus (parietal lobe)
o Brodmann’s area 3,1,2
o Controls opposite side of body
o Primary motor cortex-in precentral gyrus (frontal lobe)
o Brodmann’s area 4
o Controls opposite side of body
Cell Layers and Regional Classification of the Cerebral Cortex
o Majority of the cerebral cortex is composed of neocortex which has 6 cell layers
o Layer I- Molecular layer

Contains: dendrites and axons from other layers
o Layer II- Small Pyramidal layer

Contains Cortical to cortical connections
o Layer III-Medium Pyramidal layer

Contains Cortical to cortical connections
o Layer IV-Granular layer

Receives inputs from thalamus
o Layer V- Large pyramidal layer

Sends outputs to subcortical structures (other than thalamus)
o Layer VI- Polymorphic layer

Sends outputs to thalamus
Brodmann’s Area
o 1,2,3-Primary somatosensory cortex- postcentral gyrus- touch
o 4- primary motor cortex- precentral gyrus- voluntary movement control
o 6 sports- precentral gyrus and rostral adjacent- limb and eye movement planning
o 17-primary visual cortex- banks of calcerine fissure- vision
o 18-secondary visual cortex- medial and lateral occipital gyri- vision, depth
o 19-tertiary visual cortex- medial and lateral occipital gyri-vision, color, motion, depth
o 22- higher order auditory cortex- superior temporal gyri-form vision
o 23-27- limbic association cortex -cingulate gyrus- Emotions
o 41,42- primary and secondary auditory cortex-Heschl’s gyri- hearing
o 44, 45-Brocas- inferior frontal gyrus-speech and movement planning
Motor Systems
o Corticospinal tract- begins mainly in the primary motor cortex where neuron cell bodies project via
axons down through the cerebral white matter and brainstem to reach the SC
o AKA: pyramidal tract
o Pyramidal Decussation-crossover of fibers to the opposite side of the body which occurs at
the junction between the medulla and the spinal cord
o Lesions occurring above pyramidal decussation will cause contralateral weakness
o Lesions occurring below pyramidal decussation will cause ipsilateral weakness
o Upper motor neuron-motor neurons that project from the cortex down to SC or BS
o Lower motor neuron-located in anterior horn of gray matter of spinal or in BS motor nuclei
Cerebellum and Basal Ganglia ***KNOW ANATOMY OF THESE STRUCTURES***
o
o
o
o
o
Do not project directly to the LMN but act by modulating the output of the corticospinal and other
descending motor systems
Designed to refine movement
Receive major inputs from the motor cortex and project back to the motor cortex via the thalamus
Cerebellum, receives inputs from the BS and SC
Lesions involved ataxia (ex: PD)-abnormal coordination
Main Somatosensory Systems
1. DCML- convey proprioception, vibration sense, and fine, discrimitive touch

Primary sensory neuron axons carry information enter first the SC via the dorsal
root and then the ipsilateral white matter dorsal columns to ascend all the way to
the dorsal column nuclei in the medulla.

Then synapse onto the secondary sensory neurons which send out axons that cross
over to the other side of the medulla and ascend to the contralateral side and
synapse in the thalamus

Third order neurons project to the primary somatosensory cortex in the postcentral
gyrus.
2. Anterolateral-pain temperature sense, and crude touch

Primary sensory neurons carrying information also enter the SC via the dorsal
roots and synapse immediately in the gray matter of the SC

Secondary sensory neurons cross over to the other side of the SC and ascend in
the anterolateral white matter froing the spinothalamic tract before synapsing
in the thalamus

Third order neurons continue to the primary somatosensory cortex.
Thalamus

Important relay center

Gray matter structures located deep within the cerebral white matter just above the BS and
behind the BG

Project strongly via layer VI

Smell doesn’t go to thalamus

Receives info from cerebellum, limbic, special sensory, and reticular formation sends info to
cortical level
Stretch Reflex (Monosynaptic Stretch Reflex)

Provides rapid local feedback for motor control

Begins with specialized receptors called muscle spindles which detect the amount and rate of
stretch in muscles

Information is transmitted to the distal processes of sensory neurons and is then conveye via
the dorsal roots into the spinal gray matter

The sensory neurons form multiple synapses including some direct synapses onto LMN’s in
the anterior horn

The LMNs project via the ventral roots back out to the muscle, causing it to contract

Damage anywhere in this pathway can cause the reflex to be diminished or absent
Brainstem and Cranial Nerves ***KNOW CN****

Reticular formation of the brainstem
o Network like form central portions of the BS to from the medulla to the midbrain
o Caudal portion is mainly motor and autonomic functions
o Rostral portion is mainly regulating level of consciousness and influencing higher
areas through modulation of thalamic and cortical activity.
o Contains nuclei and white matter tracts

Midbrain

Pons

Medulla

Connections
o Rostrally-diencephalon
o Dorsally-cerebellum
o Caudally-SC
Lecture #4 9/12/14
Limbic System (fringe)

Lesions can cause
o Difficulty forming new memories
o Behavioral changes-laugh when serious or cry when funny
o Epileptic seizures caused by

Fear

Memory distortions

Olfactory hallucinations

Anatomical Location
o Cortical areas-medial and anterior temporal lobe
o Anterior insula
o Inferior medial frontal lobes
o Cingulate gyri
o Hippocampal formation
o Amygdala
o Several nuclei in medial thalamus, hypothalamus, BG, septal area and BS
o Fornix-connects hippocampal formation to hypothalamus and septal nuclei

Diverse function
o Regulation of emotion
o Memory
o Appetite
o Autonomic
o Neuroendocrine
o Olfaction
Association Cortex-functions as processing high-order information

Unimodal association cortex- higher processing takes place mostly for a single sensory or motor
modality
o Located adjacent to a primary motor or sensory area
o Ex: visual association cortex is located adjacent to the primary visual cortex

Heteromodal association cortex- involved in integrating functions from multiple sensory and or
motor modalities (ex: prefrontal association cortex)

Language-usually perceived first by the primary auditory cortex in the superior temporal lobe when
we are listening to speech or by the primary visual cortex in the occipital lobes when we are reading
o from there, cortical to cortical association fibers convey information to Wernicke’s area in
the dominant (LEFT) hemisphere

LESION: wernicke’s aphasia (receptive)
o Also goes to Broca’s area is located in the frontal lobe in the left hemisphere adjacent to the
primary motor cortex involved with muscles for speech

LESION: Broca’s aphasia (expressive)

Parietal lobe-divided by intraparietal sulcus
o superior lobe
o inferior lobe on dominant hemisphere
LESIONS

difficulty with calculations

L-R confusion

Inability to identify fingers-finger agnosia

Difficulties with written language

Gerstmann’s syndrome-a cluster of abnormalities

Apraxia-cant execute a task that is asked of them
o Spatial awareness-non dominant hemisphere

Hemineglect-neglect left side of environment/body (can see but can’t perceive)

Anosognosia-don’t think they have a disease

poor prognosis
o Extinction-eyes closed tactile or visual stimulus left side becomes “extinct” when stimulated
simultaneously

Frontal Lobe-Largest association cortices
o LESIONS-cause personality and cognitive functioning

Frontal release signs-grasp, root, suck, and snout reflexes


Perseveration-repeat a single action over and over without moving on to the next
one
Disinhibited behaviors-pervs
Abulic- stare and have delay of response
Magnetic gait- feet shuffle on the floor
Urinary incontinence-and don't care




Visual Cortex
o Parieto-occipital lobe
o Inferior temporal lobe
o LESIONS

Prosopagnosia-cant recognize faces (would have to use other senses)

Achromatopsia- “” color

Palinopsia- deja vu
Blood Supply ***KNOW ARTERIES**
1 pair of Draining Veins
o Internal jugular
2 main arteries
1.) Internal carotid
2.) Vertebral artery
a. Basilar artery

Circle of Willis consists of:
o Vertebrobasilar

Posterior cerebral arteries
o Internal cartotid

Anterior cerebral arteries

Middle cerebral arteries

Brainstem and Cerebellum
o Vertebral and basilar arteries

Superior cerebellar artery

Anterior inferior cerebellar artery

Posterior inferior cerebellar artery

Spinal cord
o Anterior spinal supplies 2/3
o Posterior spinal
CHAPTER #3
Overview of Neurologic Exam
1.) Mental status
2.) CN
3.) Motor Exam
4.) Reflexes
5.) Coordination and gait
6.) Sensory

Taking Patient evaluation, Neuro exam: diagnostics, General P.E., Patient Hx
Tying into FUNCTION!!!!
1.) Mental Status
Neuroexam.com-Video #1

Tests that have many different versions but follows a fairly standard format around the anatomy of the
brain

Involve global brain function that determine how well we will be able to perform the rest of the exam
o Apraxia
o Mood
o Logic
o Abstract reasoning

Organized around the association cortex and limbic system

Mainly dominant hemisphere (language)

r/o non dominant dysfunction (hemineglect)

frontal lobe functions- cognitive level

level of alertness, attention, and cooperation-video #4
o spelling short word and saying the months of the year front and backwards (takes 2x long
backwards)- digit span
o what is being tested? BS reticular formation and in bilateral lesions of the thalami or
cerebral hemispheres.
o Impairments in patients with: encephalitis, behavioral or mood disorders, focal brain
lesions, dementia
- A&Ox3 (video #5)
o ask the patient’s name, location, the date, and note the exact response
o what is being tested? Recent and long term memory (limbic lobe), and level of alertness,
attentiveness, and language capabilities

Memory
o Recent memory (video #6)- being able to recall items or a brief sotry after a delay of 3-5
min.

LESION in: limbic system and by the medial diencephalon medial temporal lobe
o Remote memory (Video #7)- ask the patient about historical or verifiable personal events
o What is being tested?

Anterograde amnesia

Retrograde amnesia

Language- What is being tested???

Dominant hemisphere-Brocas area

temporal and parietal lobe-wernicke’s area

subcortical white and gray matter-thalamus and caudate nucleus
o Comprehension (video #9)-how can they follow commands
o Naming (video #10): know what items are what
o Spontaneous speech (video #8)

Paraphasic speech-putting words in appropriate place (age appropriate)

Neologism-new words (ex. Wernicke’s aphasia)
o Repetition (video #11)-being able to repeat immediately (has a lot of “S” words and needs
to annunciate)
o Reading
o Writing (video #12)

Gertmann’s syndrome- patient has multiple problems with calculations (video #13), R-L confusion,
Finger agnosia, agraphia
o What is being tested? L parietal Lobe

Apraxia (video #15)-can’t execute task
o What is being tested-variable parts of the brain

Neglect and constructions (video #16)- hemineglect
o What is being tested? Right parietal lobe, frontal lobe, thalamus, BG

Sequencing tasks
o Perseveration-continual involuntary repetition of a mental act usually speech or overt
behavior
o Abulia or changes in personality
o What is being tested? -Frontal lobe

Logic and abstraction (video #22)
o Solve simple problem (take in age and education)
o What is being tested? –higher order associated cortex-not well localized

Delusions and Hallucinations (video #23)
o Toxic, metabolic, psychiatric disorders, focal seizures/lesions
o What is being tested?- association cortex and Limbic system

Mood
o Signs of depression, anxiety, mood
o What is being tested?- psychiatric in origin therefore due to imbalances in NT systems
2.) cranial nerve assessment
CNI (video #24)- olfactory-olfaction

What is being tested? Obstruction or damage to olfactory nerves in mucosa, as they cross cribiform
plate, or intracranial lesions affecting the bulb
CNII (video #25)-Optic
Visual acuity-eye chart

color vision-ability to distinguish colors (red desaturation)

visual fields (video #27)-periphery

What is being tested? Damage anywhere along the visual pathway from eye to visual cortex
CNIII-Oculomotor-extraocular muscles, pupil constrictor and ciliary muscles of lens for near vision
CNIV-Trochlear-Superior oblique muscles
CNV-trigeminal-sensations of touch pain, temp, vibration, and jt position for the face mouth, nasal, meninges,
muscles of mastication, tensor tympani
CNVI-Abducens-Lateral rectus muscle-abduction of the eye
CNVII-facial-muscles of facial expression, anterior 2/3 of tongue taste
CNVIII-vestibulocochlear- hearing; vestibular sensation
CNIX-Glossopharyngeal-taste in posterior tongue
CNX-vagus-swallowing, voice, parasympathetics to the heart
CNXI-spinal accessory-SCOM, Trap
CNXII-Hypoglossal-Intrinsic muscles of the tongue
CN examination Techniques and What’s being tested

Pupillary Response (CN II and III) video #29
o Accommodation response-converge and diverges

What is being tested?-ipsilateral optic nerve, ipsilateral parasympathetics
traveling in CN II, or pupillary constrictor muscle, or in bilateral lesion of pathways
from optic tracts to visual cortex
o Note direct and consensual response (PERRL)
o What is being tested?

Direct response (shining light into eye your testing) -ipsilateral optic nerve,
pretectal area, ipsilateral parasympathetics traveling in CN III or pupillary
constrictor muscles of the iris

Consensual Response (contralateral side)-contralateral optic nerve, pretectal
area, ipsilateral parasympathetics traveling in CN III or pupillary constrictor muscle

Extraocular movements (CN III, IV, VI) video #34
o Smooth movement
o Saccades-rapid eye movement horizontal and vertical
o Optokinetic (train)nystagmus-normal
o What is being tested? Abnormalities with central eye control which can be with individual
muscles, CN itself, cortex, and BS

Facial sensation(CN V)
o Muscles of mastication
o What is being tested? Facial sensation impaired by lesions of trigeminal nerve, trigeminal
nuclei to BS, or ascending sensory pathway to thalamus and somatosensory cortex in post
central gyrus
o Weakness in muscles of mastication due to lesions in UMN pathway synapsing on CN V in
LMN trigeminal nucleus in pons, peripheral nerve as it exits BS to muscle itself, or NM
junction

Muscles of facial expression and taste (CN VII) videos #40&41
o What is being tested? weakness caused by UMN in contralateral motor cortex or descending
pathways, LMN in ipsilateral CN VII nucleus, NM junction, or facial muscles

Unilateral deficits in taste can occur in lateral medulla or in lesions of facial nerve

Hearing and vestibular sense (CN VIII) video #42
o Vestibular sense generally not tested unless vertigo-inner ear, or limitations with gaze
o What is being tested? hearing loss=acoustic and mechanical components or ear, neural
elements of cochlea, or nerve itself. Vestibular loss=peripheral apparatus in inner ear, nerve
itself, vestibular nuclei in BS, cerebellum, or connections to occularmotor nuclei

Palate elevation and gag (CN IX, X) Video #44
o What is being tested lesion of nerve itself NM junction, or pharyngeal muscles

Muscles of articulation (CN V, VII, IX, X, XII) video #45
o Changes from baseline?
o What is being tested? peripheral or central portions of these CN; motor cortex lesions,
cerebellum, BG, or descending pathways to BS

SCOM and Trapezius muscles (CN XI) video #46
o What is being tested? SCOM or trap weakness, MN junction, LMN of CN XI; unilateral UMN
lesion in cortex or descending pathways cause contralateral weakness

Tongue muscles (CN XII) (video #47)
o Noting fasciculations of the tongue while it is resting on the floor of the mouth and have the
patient stick out their tongue to look for it move more to one side than the other
o What is being tested? unilateral weakness causes deviations toward side of weakness and
can result from lesions of tongue muscles, NM junction, LMNof CN XII, or the UMN in the
motor cortex which would cause contralateral weakness
3.) Motor Exam

Observation- looking for twitches, posture, tremors, and involuntary movement
o What is being tested? BG (resting tremor, involuntary movement) and cerebellum (active
tremor)

Inspection (video #48)-looking for muscle wasting, hypertrophy, fasciculations in hand, shoulder and
thigh (as in LMN lesions)

Palpation-palpation for tenderness noted in patients with myositis

Muscle tone testing (video 49 and 50)-patient will be relax and you will passively move move to feel
resistance or rigidity
o What is being tested? presence of UMN lesion will yield hyperreflexia and increased tone
due to damage to pathways that travel in close approximation with the corticospinal tract;
also BG and cerebellum

Functional testing (video #51 and 52)-performed before specific muscle testing
o Drift- holding arms up and close eyes and muscle weakness in UE limb shows “drifting” away
o Fine movements- testing rapid finger tapping, rapid hand pronation-supination, rapid
hand/foot taping

Strength testing (Videos #54-57)- testing in symmetrical fashion and compare with opposite side
o What is being tested? patterns of weakness can help localize to particular cortical or white
matter region, SC level, nerve root, peripheral nerve or muscle
4.) Reflexes (video #58)-DTR

limbs are relaxed and symmetrical and tested bilaterally

clonus-seen when reflexes are very brisk. A repetitive vibratory contraction of the muscle that occurs
in response to muscle and tendon stretch

rated:
o 0-absent (abnormal)
o 1+-trace or seen only with reinforcement
o 2+-normal
o 3+-brisk
o 4+-non-sustained clonus (abnormal)
o 5+-sustained clonus (abnormal)

what is being tested? Diminished abnormalities in muscles, sensory neurons, LMN, and NM junction,
acute UMN lesions and mechanical factors such as joint disease are due to UMN lesions

plantar response (Babinski’s-video #60)-UMN lesion; documentation using a picture stick figure and
reflex responses
5.) Coordination & gait (video #62)

Appendicular coordination tests-fine movements of the hands and feet
o rapid alternative movement
o heel-shin test
o finger-nose test-looking for accuracy
o what is being tested? testing multiple integrative sensory and motor subsystems that
include

position, sense pathways, visual pathways, LMN, UMN, BG, Cerebellum

Rhomberg test (video #67)
o What is being tested? integration of visual, vestibular, and somatosensory systems

Gait-gait
o Observe from front and lateral views and note:

Stance-how far apart feet are

Circumduction-an abnormal arced trajectory of leg swing in the medial to lateral
direction)

Tandem gait

Forced gait-asking them to walk on toes, insides/outsides of feet

What is being tested? multiple sensory or motor systems which include:

Vision, Proprioception, Vestibular, LMN, UMN, BG, cerebellum, higher
order planning systems in association cortex
6.) Sensory Exam

Primary sensation, asymmetry, sensory level (video #70)
o Light touch
o Pain-sharp/dull
o Temperature
o Vibration
o Joint position sense
o Two point discrimination

Cortical sensation; extinction (videos #75-77)
o Graphesthesia- writing letter or number on hand
o Sterognosis-closes eyes and recognizing common objects
o Tactile extinction-too much stimulus so info on lesion affected side is not perceived
o What is being tested? Peripheral nerves, nerve roots, posterior columns, anterolateral
systems in SC, BS, Thalamus, or sensory cortex
Neurologic Exam as a Flexible Tool

Flexibility-prioritize

Exam limitations and strategies- impairments in one area affect performance in other portions of exam
Coma Exam

Simpler exam

Performed in emergency situations

Useful on uncooperative patients

1.) Mental status- document with specific statement of what the patient did in response to a stimulus

2.) CN assessmento Opthalmoscopic exam (CN II)
o Vision (CN II)
o Pupillary Response (CN II, III)
o Extraocular Movements and vestibule-ocular reflex (CN III,IV, VI, VIII)
o Corneal Reflex, facial asymmetry, grimace response (CN V, VII)
o Gag reflex (VN X, IX)

3.) Sensory and 4.) Motor exam
o spontaneous movements
o withdrawal from a painful stimulus

5.) Reflexeso DTR
o Plantar response
o
Posturing reflexes

6.) Coordination and Gait-not testable
Brain Death-a clinical Diagnosis

irreversible lack of brain function

no evidence of brain/brainstem function

two separate brain death examinations confirm diagnosis
Conversion Disorder, Malingering, and Related Disorders

Psychiatric disorders mask themselves as neurologic dysfunction
o Larger classification-think they genuinely have disease

Conversion disorder-causes patient to have sensory or motor deficits without a
corresponding focal lesion in NS

Somatization disorder-patients have multiple somatic complaints that change over
time
o Second, less common classification- have conscious control over symptoms, ulterior motive

Factitious disorder-Dr. Shop, internally driven (Munchausen syndrome)

Malingering-externally driven, (ex. Work comp)
Chapter #4 9/15/14
Medical history

Ask the right questions

Listen observe

Don’t leave yourself guessing
Components of Neurological Exam

Mental status

CN and sensory organs

Motors systems

Reflexes

General sensory systems

Gait
Neurologic Diagnosis

where is the lesion

what is the lesion
o differential diagnosis-confirm with diagnostic tools
Imaging planes

Horizontal

Coronal

Sagittal

Scout (localized)-horizontal with a slight angle
Computerized Tomography

Advantages
o Greater sensitivity than plain x-ray
o Optimal for bony lesions

Disadvantages
o Ionizing radiation
o Poor choice for posterior fossa lesions-distortion
o Contrast allergy-iodine

30k 2-4 mm x-ray beams computed into a single image

x-ray beam is rotated around the patient to take many different views of a single slice of the patient

data is reconstructed by a computer to obtain a detailed image of all the structures in the slice

amount of energy absorbed depends on the density of the tissues
o hyperdense-whiter (bone)

calcium

metal

blood
o hypodense-darker (fat)

air

gliosis-scar tissue

tissue loss

edema

white matter is darker than gray matter due to myelination
o isodense-gray (CSF)

can be used to visualize a variety of different intracranial abnormalities
o cerebral infarctions

cannot be seen y the CT in the first 6-12 hours

cell death and edema leas to an area of hypodensity seen near the distribution of the
area of ischemia

there will be distortion of the local anatomy due to the edema (longitudinal fissure)

over weeks to months, the brain tissue may be present as a result of gliosis and
brain necrosis replaced by CSF
o neoplasms

may appear hypodense, hyperdense, or isodense depending on the type and stage

may contain areas of calcification, hemorrhage, or fluid filled cysts

edema (hypodense)

IV contrast dye is helpful in this diagnosis
o mass effect

any thing that distorts the brain’s visual anatomy by displacement

can occure with edema, neoplasm, hemorrhage

detected by compression of the ventricles, effacement of the sulci, loss of cortical
structure
o hemorrhage: depends on how recently it has occurred.

Fresh ICH coagulates immediately and shows up as hyperdense.

As clot is broken down after a week it becomes isodense

After 2-3 weeks it becomes hypodense
Magnetic Resonance Imaging

Strong magnetic field aligns protons along the longitudinal orientation of the applied field

A radiofrequency pulse shifts the proton alignment axis from the longitudinal to transverse planes

When the RF pulse is stopped, the protons realign to the applied magnetic field

The radiofrequency energy that was absorbed and then released results in an electric current that is
detected by the electromagnetic receiver coils

ICH goes under changes on MRI images
o First 6-24 hours- T1 gray, T2 light Gray
o 1-5 days- T1, Gray, T2 Dark Gray
o 3-7days- T1 White, T2 Dark gray
o 3-30 days- T1 White, T2 white
o >14 days- T1 dark gray, T2 black

T1
o Best of anatomy details
o CSF is black

T1 with contrast
o Shows inflammatory, vascular and some neoplastic lesions

T2
o Best for white matter lesions (MS)
o CSF white

FLAIR
o Same as T2 but with CSF subtracted

Diffusion with weighted
o Shows the movement of water across membranes
o Altered when Na, K, ATP dependent pump damaged (anoxia)

Advantages
o High resolution
o No ionizing radiation
o Contrast allergy is rare
o No bony artifacts

Disadvantages
o Requires patient cooperation
o Cannot be used with ferromagnetic implants (pacemaker, bladder stimulus, cochlear implant)
o Contrast-induced renal damage
o Costs

CT vs T2 weighted MRI
o Bright on T2 MRI dark on CT
o Dark on T2 MRI bright on CT
o Except

fat-bright on CT and T2

Blood <48 hrs-dark on T2

Blood > 48 hours bright on T2
Positron Emission Tomography

Measures regional concentration of systemically administered tracers (eg18F-deoxyglucose, H2 15O)

Expensive as requires a linear accelerator

Applications include grading brain tumors, distinguishing types of dementia, confirming PD

Often used in Oncology

$$$$$

Red= High metabolism of glucose

Blue/purple=low metabolism of glucose (common in Alzheimer’s patient in the frontal and parietal
lobe)
Functional MRI

Localizes cerebral activity in healthy vs diseased brains=look at differences (diseased should have
more surface area due to it working harder in that area)

Based on flood flow (hemoglobin concentration)

Advantages of PET
o Non invasive
o Higher resolution
Doppler US


can be used to measure flow and lumen diameter of large BV in the head and neck
most useful for assessing the proximal internal carotid to help with decisions for possible surgery in
carotid stenosis

accurate and harmless

smaller arteries cannot be assessed

often used in ICU to detect vasospasm following subarachnoid hemorrhage

cannot detect aneurysms or other vascular abnormalities
Neuroangiography

used to visualize lesions of the BV

used with other imaging techniques such as x-rays, ct, or MRI

evaluates for CVD, aneurysms, vascular malformations

invasive-undergo local anesthesia and catheter is inserted in the femoral artery to aorta under x-ray
guidance where dye is injected
Electroencephalography

measures brain electrical activity of cortical neurons that are regulated by subcortical structures and
used in the diagnosis of epilepsy, metabolic disorders, sleep disorders

alpha rhythm seen posteriorly when eyes closed and patient is relaxed
Electrodiagnostics: Evoked potentials

measures conduction velocity in special sensory (visual evoked, auditory evoked) and general sensory
(somatosensory evoked) pathways

used in MS (visual-evoked)

BS or SC lesions
Electromyography

Measures electrical activity in muscles

Monpolor needle electrodes

Surface electrodes

Looks at neuropathic vs myopathic changes
Nerve conduction studies

Measures velocity of nerve conduction

Assists in diagnosis of peripheral nerve problems such as demyelination and entrapment

Only large nerves evaluated (1A alpha)

Measure how long AP gets to recording electrode
Lumbar Puncture

Spinal tap

Obtain CSF

Analyze color, cell count, protein and glucose level

Special test for specific diagnostic considerations (MS, malignancy)

Normal
o Glucose 2/3 serum glucose
o Protein 25-45
o Cells < 8 monocytes

Bacterial meningitis
o Glucose <40
o Protein 100-500
o Cells 1k- 10k (90% PMNL’s)

Viral meningitis
o Glucose N
o Protein slightly elevated
o Cells <100 Monocytes

Tuberculosis
o Glucose <40
o Protein 100-200
o Cells 100-300 (<50% PMNL’s)

Ca meningitis
o Glucose <40
o Protein 100-200
o Cells N to slightly elevated (malignant cells)