1. Localization in Neurologic Diagnosis Part 1
D. Joanne Lynn, MD
Associate Professor of Neurology
Associate Dean of Student Life

2. Objectives
Be able to accurately differentiate between examination findings suggesting upper vs. lower motor neuron pathology
Correlate neurologic signs and clinical features to the appropriate level of the neuroaxis for the following neurologic localizations:
Focal cortical disease, including a gross classification of aphasias;
Cerebellar disease;
Brainstem lesions;
Spinal cord disease;
Root and peripheral nerve disease;
Neuromuscular junction dysfunction;
Myopathy

3. Objectives – continued…
Define dysarthria, dysphagia, aphasia, aphonia. Compare and contrast Broca’s, Wernicke’s, conduction and global aphasia.
List the primary functions of the frontal, parietal, temporal, and occipital lobes.
Correlate visual field deficits with lesions along the visual pathways.
Describe abnormalities of clinical eye movements that will be caused by lesions in cerebral and brainstem pathways that control eye movements.
Recognize clinical presentations that suggest brainstem pathology: grouped cranial nerve palsies, crossed motor and sensory findings.
Recognize clinical syndromes related to spinal cord pathology based on examination findings of motor and sensorydeficits.
Identify motor, sensory and reflex abnormalities that occur in C6, C7, C8, L5 and S1 radiculopathies.

4. Holism vs. Cortical localization
Holism – all parts of the brain are similar in function, undifferentiated and work together as an aggregate field
Localism – the concept that specific neurons and areas of the brain have specific functions
Connectionism – a view that mental or behavioral phenomena are the product of interconnected networks of simple units.
Early conceptions of the brain and brain function included ‘Holism’ – a concept that the brain was fairly undifferentiated tissue that worked together to perform all functions. Through various observations, holism gradually gave way to localism – an understanding that specific neurons, structures and brain areas are specialized and have specific functions.
Extreme localism and holism have both been replaced by "connectionism." This view contends that lower level or primary sensory/motor functions are strongly localized but higher-level functions, like object recognition, memory, and language are the result of interconnections between brain areas functioning as networks.

5. Cortical Localization vs. Holism
Phineas Gage – 1848
Broca and M. Leborgne – 1861
Wilder Penfield – electrical stimulation results
Animal ablation studies
Functional studies by PET – 1990s
I would like to just mention a few major steps in the development of our understanding of localization of specific functions in the nervous system.
Phineas Gage – the case of a railway worker whose tamping iron pierced through his frontal lobes causing a peculiar change in his personality
Paul Broca’s case study of his patient Monsieur LeBorgne and the type of aphasia associated with his left frontal lobe stroke. Wernicke’s studies of aphasia patients also supported ‘localism’.
Dr. Wilder Penfield was a neurosurgeon at the Montreal Institute who did some of the earliest surgeries for epilepsy. He used the opportunity of each surgery to explore localization by stimulating different cortical sites and observing what motor or sensory responses were reported by the patient.
Animal ablation studies were used to confirm early patient observations.
Imaging and more recently functional imaging by PET and functional MRI scans have deepened our understanding of localization of specific functions in the nervous system.

6. Phineas Gage and the frontal lobe
This is a picture that shows the skull of Phineas Gage with a defect in the left frontal bone and the actual tamping rod that shot through the frontal lobe. Phineas Gage miraculously survived the traumatic brain injury in an age without antibiotics but was forever changed in personality (and not for the better!).

7. Paul Broca and M. Leborgne’s brain
These are pictures of Professor Broca and his patient Monsieur Leborgne’s brain.
After his stroke, Monsieur Leborgne could understand language but could not speak (could only say "tan"), In 1862, Broca studied this patient’s motor aphasia and then correlated the clinical symptoms with the area of injury in the left frontal lobe at autopsy examination. He found this lesion in several other patients with motor type aphasia supporting the theory of localism.

8. Learning localization via pathological observations
This specimen shows an example of the type of correlative observations that were required to initiate our understanding about localization in the nervous system. In this case Dr. Spiller saw a patient with unilateral loss of pain sensation. Later, autopsy examination showed a tuberculoma in the contralateral anterolateral column which disrupted the ascending anterolateral spinothalamic tract.

9. Wilder Penfield and Cortical Mapping
Dr Wilder Penfield, born and educated in the U.S., eventually worked at the Montreal Neurological Institute as a neurosurgeon. With his colleague, Herbert Jasper, he invented the Montreal procedure, in which he treated patients with severe epilepsy by destroying areas of the brain where the seizures originated (seizure focus). Before resecting tissue, he stimulated the brain with electrical probes while the patients were still conscious, and observed their responses.
He was able to map the sensory and motor cortices of the brain and produced the cortical homunculi maps that we still use today.

10. Penfield and cortical mapping
Penfield at work! And a drawing of his homunculus.

11. PET scan and mapping
This picture gives you an idea about some of the advances in cortical localization that came about through the use of PET scan functional imaging. Notice that simple movements of the left and right fingers activate the motor cortex. More complex movements activate multiple areas of cortex. Even imagining making a movement of the fingers activates various locations of the cortex. Functional imaging technology continues to improve and allow more detailed understanding of brain function.

12. Localization in neurologic diagnosis
Joanne Lynn MD
Localization in neurologic diagnosis
Now let’s move on to the process of localization in neurologic diagnosis. Localization is a process that is must be done to determine the site of the pathologic process involving the nervous system. The nervous system spans from cerebral cortex to nerves and muscles in the toes and we can’t just throw a person in the MRI scanner and scan the whole body each time they have a neurologic complaint. Instead we must deduce the site of the lesion from clues in the neurologic history and examination to guide further studies. Clinicians who decide to specialize in neurologic disease often enjoy the challenge of this type of analysis and appreciate the fact that the examination plays an important role in understanding the disease even in this age of high tech imaging.

13. Levels of the nervous system
Central Nervous System
Cerebrum / cortex
Basal ganglia
Cerebellum
Brainstem
Spinal Cord
Peripheral Nervous System
Roots
Plexus
Peripheral nerves
Neuromuscular junction
Muscle
Physicians can use the neurologic history and examination to localize a lesion to various levels of the neuroaxis or span of the nervous system. The nervous system spans from the cortex all the way down to the muscles of the limbs. The purpose of this lecture is to review the anatomy, neurologic symptoms and examination findings that allow one to localize to one of these levels accurately. The gross levels of the neuroaxis are listed in this slide and the first differentiation is between central and peripheral nervous system levels.

14. Anatomical Localization
History and physical examination
Can the findings be explained by:
One lesion?
Multiple discrete lesions?
A diffuse process?
What level / levels of nervous system are affected?
Beware false localizing signs, non-physiologic (functional) disease
As one approaches a patient with neurologic complaints or findings, one should ask several questions.
What does the history and examination show?
And can the symptoms and/or neurologic findings be explained by
One single lesion?
Multiple discrete lesions? (like Multiple sclerosis)
A diffuse process (like a metabolic or toxic condition such as hypoglycemia, hyponatremia, a toxin)?
3) What levels or levels of the nervous system are affected?
4) Always keep in mind false localizing signs – such as a 6th nerve palsy from increased intracranial pressure rather than a lesion directly on the abducens nucleus or CN VI. Also keep vigilant about psychogenic findings such as functional weakness, sensory complaints – findings that don’t seem to obey neurologic rules.

15. Levels of the nervous system
We will use this simplified diagram of the nervous system and discuss major neurologic exam findings at each level.

16. Let’s start at the top with the cerebral cortex
We are going to start up at the top with the cerebrum and its cortex and work our way down the neuroaxis.

17. Important cortical areas for clinical diagnosis
Please review the important cerebral cortical areas that control important neurologic functions that may be impaired in various neurologic disorders and detected on the neurologic examination.
Frontal lobe motor strip
Parietal lobe sensory areas
Frontal motor speech area
Wernicke speech area
Visual cortex

18. Cortical Functions - Language
Aphasia/dysphasia – true language disturbance with errors of grammar, word production and / or comprehension
This should be differentiated from disorders of speech production:
Dysarthria – disorder of articulation due to the motor function underlying speech in which language is intact
Dysphonia – impairment of the ability to produce sounds due to disorder of larynx or its innervation
Aphonia – total loss of voice often due to bilateral recurrent laryngeal nerve injury, resection of larynx, etc.
I would like you to learn to differentiate aphasia from several other terms – dysarthria and dysphonia.
Aphasia is a true disorder of language and refers to impairment of the production and/or comprehension of written or spoken language. Aphasia is most often caused by lesions (especially strokes) of the dominant cortex but may also result from lesions in deeper brain areas such as the thalamus.
Dysarthria – this term refers to an impairment of articulation due to difficulty with the motor function/ coordination underlying speech without impairment of comprehension or language production. Facial weakness, cerebellar dysfunction, basal ganglia disease can all cause dysarthria.
Dysphonia – refers to the loss of voice due to a disorder of the larynx or its innervation. This can vary from mild hoarseness to the loss of voice from a laryngectomy. Aphonia is the total loss of voice often from a bilateral recurrent laryngeal nerve injury or laryngeal disease.

19. Cerebral Dominance / Lateralization
90% of the population is definitely right handed
99% of these are strongly left hemisphere dominant for language
The 10% who are left-handed are different:
80% have some degree of language representation in both hemispheres
As you know, language deficits can help to localize a lesion. Ninety percent of the of the population is right handed and the vast majority of right handers are strongly left hemisphere dominant for language. This is a help with localization and is why neurologists start their H&Ps with “this is a 67 year old right handed man who….”
The 10% of the population who are left handed will often have a dominant right hemisphere but a significant portion will have some language representation in both hemispheres.

20. Language testing Handedness
Spontaneous speech: fluency, articulation, prosody, grammar, errors (paraphasias)
Comprehension: single words, yes/no questions, complex commands
Repetition
Naming
Reading/ Writing
Language testing on neurologic examination includes the assessment of the items above.

21. Broca’s aphasia Lesion in dominant inferior frontal gyrus
Nonfluent aphasia
Comprehension good
Associated contralateral hemiparesis if nearby motor strip is involved
Broca’s aphasia (expressive, motor, anterior aphasia) results from a lesion in the dominant hemisphere inferior frontal gyrus. These patients have a drastic loss of speech fluency (as low as 10 to 12 words per minute). Their speech is slow, halting, effortful with loss of grammar and small transitional words such as ‘and’ and ‘then’. Comprehension is preserved. These patients are often frustrated by their deficit. Weakness of the right arm and right face is usually associated.

22. Wernicke’s aphasia Lesion in dominant superior temporal gyrus
Speech fluent but nonsensical
Poor auditory comprehension
Poor awareness of problem
Wernicke’s aphasia may be called a receptive, sensory or posterior aphasia. It is due to damage to the left auditory-association cortex. Although speech is effortless and fluent, it is often unintelligible because of frequent errors in word and phoneme choice. These patients have trouble comprehending others.

23. Aphasia- Localization
Just a quick reminder of the locations of Broca’s and Wernicke’s areas.

24. Vascular supply related to aphasias
Broca's, Wernicke's and other focal aphasias are often caused by strokes. I like this diagram because it shows you the middle cerebral artery and how it divides into an inferior and a superior division. Broca's area is served by the proximal superior division which goes on to serve the motor strip on the lateral aspect of the cerebral hemisphere. The inferior division of the MCA courses back to serve the parietotemporal region which includes Wernicke's area.

25. Frontal Lobe Hemiparesis
Personality changes: Apathy, euphoria, jocularity, irritability, social inappropriateness
Decreased executive functions
Frontal micturation area – 2nd frontal gyrus – may develop urinary incontinence (as in NPH)
Disorders: tumors, head trauma, hydrocephalus
Tests: alternating sequences
alternating motor patterns
` fist-palm-side test
This is offered as a brief review of frontal lobe functions. The frontal lobe is very large and lesions in different areas can have markedly different clinical manifestations.
The most obvious is hemiparesis if the motor strip or other motor areas are affected – this can very from a very subtle pronator drift to a dense hemiplegia (paralysis on one side).
Patients with frontal lobe disease typically do not show dramatic cognitive deficits but will often develop specific personality changes that might include: apathy, disinhibition, excessive and inappropriate jocularity (witzelsucht), irritability, poor tolerance of frustration, poor planning . These changes are related to impairment of executive functions - The executive functions of the frontal lobes involve the ability to recognize consequences (future results from current actions), to choose between good and bad actions to suppress socially unacceptable responses, and to determine similarities and differences between things. If the frontal lobe is injured these functions maybe impaired.
Urinary incontinence – there is a frontal micturation center which helps to suppress the reflex for urinary voiding. Injury to this center may cause urinary incontinence as in NPH.

26. Descending Corticospinal and Corticobulbar tracts
This slide is to remind you that one of the most important set of long tracts originates in the frontal lobe – the corticospinal and corticobulbar tracts. The corticospinal tracts originate in upper motor neurons in the motor strip, descend through the posterior limb of the internal capsule, travel in the cerebral peduncles of the midbrain, the base of the pons, and the base of the medulla, crossing at the pyramids of the lower medulla and then traveling down the lateral aspect of the spinal cord. These upper motor neurons (UMNs) eventually synapse with lower motor neurons in the ventral horn of the spinal cord. The corticobulbar tract originates in the motor strip and travels with the corticospinal tract giving off fibers to various cranial nerve motor nuclei at each level of the brainstem.

27. Alternating sequencing tasks – impaired in extensive frontal lobe disease
This slides shows abnormalities in the ability to perform alternating sequencing tasks in patients with frontal lobe disease. Drawing A models alternating square and triangular items. The patient tries to reproduce the drawing below but is unable to do this accurately. In item B, the drawing is of alternating 'm' and 'n'. Again the patient is unable to accurately and discretely produce these alternating sequences.

28. Frontal lobe function: alternating sequences: Fist, side, palm
Another test of frontal lobe function – alternating sequences is to ask the patient to rapidly show in a sequence the fist, side, and palm of the hand to the examiner. People with frontal lobe injury may be unable to do this consistently.

29. Temporal Lobe Bilateral lesions: profound memory loss
Dominant side: decreased verbal learning
Nondominant side: decreased visual learning
Visual field defects
Most common site of seizure focus for partial seizures
Temporal lobe injuries will most often result in deficits in learning and memory.
Bilateral anterior temporal lobe lesions can cause short-term memory loss.
Unilateral anterior temporal lobe lesions can interfere with verbal or visual learning – the extent depends upon whether the lesion is in the dominant or non-dominant temporal lobe.
Superior quandrantanopias can result from temporal lobe lesions.
The temporal lobe is the most common site for a seizure focus.

30. Temporal lobe and memory
A visit to the hippocampus bar may interfere with memory and cause temporal discontinuities.

31. Parietal Lobe
Either side: disturbance of sensation on the opposite side of the body
Central sensory functions:
Decreased 2 point discrimination
Sensory inattention / extinction
Sensory agnosia:
Astereognosis
Agraphesthesia
The parietal lobe contains the primary somatosensory cortex located in the postcentral gyrus. Information about the primary sensory modalities are carried to the thalamus via the posterior columnp medial lemniscal and anterolateral (spinothalamic) pathways. From the thalamus, another relay neuron, brings sensory information to the parietal somatosensory cortex. Complex processing and integration of sensory information of multiple different modalities occurs in the parietal lobe which allows spatial sense and navigation. There is lateralization with the left parietal lobe specializing in symbolic functions such as mathematics and language and the right parietal lobe permitting production of images and the understanding of maps.
Extinction is an impairment of the neurologic ability that allows the brain to pay attention to two stimuli at once. This may be seen in cerebral lesions outside the parietal lobe but is most prominent in parietal lobe pathology.
Interestingly, the parietal lobes have also been found to the site to which 'self- transcendance' localizes - a personality trait that determines predisposition to spirituality.

32. Parietal Lobe Spinothalamic tract Pain pathways – to thalamus
To parietal lobe
Parietal lobe – This is a good time to review two ascending long tracts that bring sensory information to the parietal lobe.
This slide is to remind you of the importance of the spinothalamic tract bringing pain and temperature information from the other side of the body to the VPL nucleus of the thalamus. A higher order neuron then relays the sensory information to the parietal lobe.
Remember – small diameter and unmyelinated pain fibers carrying pain and temperature information enter the spinal cord via the dorsal horn root entry zone. These axons synapse on a second neuron in the gray matter of the spinal dorsal horn. Please note and remember that the axons of the second order neurons cross in the ventral gray of the spinal cord at the approximate level where the pain fibers enter the dorsal horn of the spinal cord and then ascend in the spinothalamic tract. Please trace this pathway from entry of pain fibers in the cord up to VPL nucleus in the thalamus and then to the parietal lobe. You can also see where pain and temperature sensory fibers from the face enter the medulla, cross over and ascend to the contralateral VPM nucleus of the thalamus. The VPM also projects to the parietal lobe.

33. Parietal Lobe Vibration and proprioception input
Posterior or dorsal columns
To Nucleus gracilis
and cuneatus
To Thalamus
To Parietal lobe
Parietal lobe – review the dorsal column-medial lemniscal tracts.
This slide is to review for you the dorsal column long tracts that end up bringing vibration and proprioception information to the parietal lobe. Note that sensory information enters the dorsal horn, ascends in the dorsal columns on the same side to N. gracilis and cuneatus. The second order neuron crosses in the lower medulla and ascends to the VPM nucleus of the thalamus. A third order neuron then takes the information to the parietal lobe.

34. Parietal Lobe Syndromes
Dominant hemisphere:
Apraxias – inability to carry out an action in response to verbal command in the absence of problems with comprehension, impairment of motor function.
Gerstmann’s syndrome: impaired calculation, left-right confusion, finger agnosia, dysgraphia
Nondominant hemisphere:
Neglect of opposite side
Impaired constructional ability
Lesions of the dominant parietal lobe (and sometimes other lobes on the dominant hemisphere) can cause various types of apraxias.
An apraxia is an inability to carry out an action in response to verbal commands in the absence of problems with comprehension, motor function or coordination.
Gerstmann’s syndrome is a special syndrome most often caused by injury to the dominant inferior parietal lobule and it consists of a tetrad of neurologic findings: impaired calculation (assuming that the person could perform calculations before the injury), left-right confusion or disorientation, finger agnosia (difficulty identifying each finger or differentiating an index finger from a ‘pinkie’) and trouble writing.
Lesions of the non-dominant hemisphere (and most often but not always the parietal lobe) may be associated with neglect of the opposite side of the body and environment and impaired constructional ability.

35. Neglect – parietal lobe dysfunction
Parietal lobe functions
The parietal lobe integrates all of the primary somatosensory information that comes to it. It also performs higher integrative sensory functions and networks with other systems. If the parietal lobe is injured (such as the non-dominant right parietal lobe here), neglect for the left side of the world may be striking. Here the patient was asked to write and to construct a clock and neglect for the left side is present.

36. Occipital lobe
The primary function of the occipital lobe is integration of visual input.

37. Visual system Optic nerves, tracts, Radiations and cortex
And associated
visual field
defects
It is more important for the purpose of localization of lesions to learn the pathways of the visual inputs from retinal to occipital lobe and to know what type of visual field defect derives from interruptions of the pathways at various sites.
Amaurosis of one eye – lesion to optic nerve
Complex lesion of the genu of optic chiasm (not important to learn)
Bitemporal hemianopia – optic chiasm
Homonymous hemianopia – lesion of optic tracts
Homonymous quadrantanopia
Inferior visual field loss – parietal lobe optic radiation lesion
Superior visual field loss – temporal lobe optic radiation lesion
Homonymous hemianopia – occipital lobe lesions, may have macular sparing.

38. Laughter is the best medicine
You are supposed to laugh!

39. Basal ganglia
A whole set of clinical neurologic problems may be associated with lesions of the basal ganglia.
Clues to this localization include:
Some types of tremor
Rigidity
Hypokinesia or hyperkinesia
Postural disturbances
Many movement disorders caused by dysfunction in this system are not associated with dramatic abnormalities on routine imaging – so the clinician must recognize typical syndromes by clinical features on history and exam.

40. Cerebellum Cerebellum
Let’s talk about signs that localize a lesion to the cerebellum as we come down the neuroaxis….

41. Cerebellum – clinical signs
Incoordination
Dysdiadochokinesis
Terminal dysmetria
Intention tremor
Truncal and appendicular
ataxia
Hypotonia
Rebound
Oculomotor abnormalities
Dysarthria
The word cerebellum means “little brain” and it provides excitatory outputs to the cerebral hemispheres, brainstem, and basal ganglia to help coordinate movement, balance and motor learning.
Injury to the cerebellum leads to the following signs on neurologic examination:
Incoordination – poor coordination of movements
Dyskiadochokinesis – impaired performance of rapid alternating movements such as screwing in a light bulb, foot tapping
Terminal dysmetria – “overshoot” when pointing at an object
Intention tremor- a tremor that worsens as the limb approaches a target (as in finger to nose testing)
Ataxia – truncal and appendicular
Hypotonia – severe cerebellar disorders can lead to pathologic decreases in tone
Rebound – this is a phenomenon in which a muscle group that is contracted against resistance that is suddenly removed, the antagonist muscle fails to check the movement and compensatory agonist relaxation does not occur.
Oculomotor abnormalities – cerebellar lesions can be associated with nystagmus as well as some even more unusual eye movement abnormalities.
Dysarthria – slurred speech, sort of like severe alcohol intoxication
commons.wikimedia.org

42. Ataxia
Incoordination or clumsiness of movement not caused by weakness or sensory loss – rather caused by a disordered contractions of paired agonist and antagonist muscles
The word ataxia derives from Greek words meaning ‘lack of order’
Localization:
True ataxia is Cerebellar
Sometimes people speak of Vestibular ataxia or Sensory (proprioceptive) ataxia because they are also associated with staggering gait/ loss of balance
So beware that this is a word that may mean different things to different speakers
Ataxia is a word for incoordination or clumsiness of movement. Normally our fine coordination derives from the way that the cerebellum uses antagonistic muscle groups for fine-tuning of movements. The word derives from the Greek word for 'lack of order.' Ataxia is classically a word that refers to a cerebellar disorder. However, there are other problems that look like cerebellar ataxia so the word is sometimes applied to incoordination due to sensory deficits or gait disorders due to vestibular problems.

43. Cerebellar modulation Of descending Corticospinal tract
Cerebellar connections with the corticospinal tract. Injury to one of the cerebellar hemispheres is associated with cerebellar signs such as incoordination and cerebellar tremor on the same side of the body as the injury. This diagram demonstrates the 'double crossings' in the system that lead to ipsilateral deficits.
Note the corticospinal tract that starts in the cortex and crosses in the lower brainstem. But also note that there are corticopontine fibers that transmit information to the opposite cerebellar hemisphere for input and influence on signals controlling movements. This information is then transmitted back up to the opposite cerebral cortex where it modulates the output of the descending corticospinal tract.
So if you have an injury to the left cerebellar hemisphere, it will affect the output back up to the right cerebral cortex and via the corticospinal tract, the motor control for the left side of the body.

44. Brainstem level localization
OK, Now leaving the Cerebrum and cerebellum
We shall now talk about the brainstem.

45. Brainstem – Clues to Brainstem Localization
Grouped cranial nerve findings
Brainstem site
Site within skull
Generalized disorder of nerve, NMJ
Divergent eye movements with diplopia
Vertigo
Discrepancies in lateralization of motor or sensory deficits – alternating sensory or motor findings
Look for well-defined syndromes – like brainstem strokes
the brainstem is much too complex to cover in detail here. The main clues that should alert you to the possibility of a brainstem lesion are:
Grouped cranial nerve deficits
Divergent eye movement abnormalities - diplopia. There can be a lot of different causes and localizations for diplopia but brainstem is one of them. Judge it by the company that it keeps! (That is, is the diplopia occuring in association with any other brainstem findings?)
Vertigo (although this could be vestibular apparatus and not in the brainstem). Vertigo is very common and usually peripheral but consider a brainstem problem in the differential.
Discrepancies in lateralization of motor or sensory findings (alternating weakness and/or sensory loss on face compared with body)
Well defined brainstem syndromes such as brainstem stroke findings.

46. Brainstem wiring for eye movements
Brainstem control of eye movements
This diagram shows that input comes from the cerebral hemisphere to initiate a bilateral eye movement (either voluntary saccades or pursuit movements). This signal crosses the midline and then innervates the PPRF (paramedian pontine reticular formation) or pontine lateral gaze center in the pons on the opposite side. This center sends neurons to CN VI on the same side to innervate that lateral rectus muscle to tell the eye to abduct. That PPRF also sends signals to the CN III nucleus on the opposite side via the MLF (median longitudinal fasciculus) to tell the opposite medial rectus to cause the other eye to adduct.
If the PPRF/ CN VI area is destroyed on one side by a stroke, the patient cannot look to the side of the lesion.

47. Joanne Lynn MD
Facial palsies – Please localize as Upper vs. Lower motor neuron lesions
Remember that this is an important localization – whether a facial palsy is due to an UMN or LMN lesion.
A central facial palsy (or UMN facial palsy) is due to a lesion that is above the facial nucleus. It affects either the UMN cell bodies in the cortical motor strip or the descending UMN axons in the corticobulbar tract that will synapse on the facial nucleus. If we have a tumor or stroke involving one hemisphere and its motor strip or descending corticobulbar tract, we will have weakness in a central pattern affecting the lower half of the opposite side of the face because the corticobulbar fibers cross as they move through the brainstem. However, the forehead will be spared and be able to wrinkle because the upper part of the facial nucleus which serves the forehead receives UMN corticobulbar innervation from both cerebral hemispheres where as the lower part of the facial nucleus only receives corticobulbar fibers from the opposite cerebral hemisphere.
A peripheral facial palsy (or LMN facial palsy) is due to a lesion involving the facial nucleus of the fibers of the facial nerve after they leave the facial nucleus. If the nerve is hurt, all muscles on the side of the face ipsilateral to the facial nucleus or nerve will be affected. Peripheral facial palsies are often more severe in terms of weakness than central facial palsies.
Why does this matter? If you have a central facial palsy, the doc should start ordering a head CT or brain MRI to assess for stroke or mass lesion. If you only have a peripheral palsy, they will think about whether you have something bad like Lyme disease if you live in a Lyme area but otherwise will just consider giving you some steroids and/or antiviral agents for Bell’s palsy, send you home without imaging to follow-up with your primary care provider. Most of these improve with time.

48. Facial palsy on the right….
A video would help, wouldn’t it? In the office or ED, you will just ask the person to wrinkle up their forehead, squeeze their eyes shut, show all their teeth, stuff like that and you will be able to see what muscles are weak.

49. Left facial palsy Woman with a peripheral facial palsy – note that the
Left side of the
forehead does
not wrinkle while the
right does.
a woman with a peripheral facial palsy.

50. Brainstem stroke syndromes and localization
OK, we are not going through the brainstem stroke syndromes again but this is to remind you to have some awareness of typical brainstem strokes.

51. Midbrain stroke syndromes
If it is a stroke syndrome with a CN III palsy, then it involves the midbrain.

52. Laughter is the best medicine
Again, so a small chuckle would be appropriate at this point. Failure to generate a smile or chuckle might imply a frontal lobe lesion with impairment of emotional expression / abulia.
Or maybe you are just tired of all this neuro!

53. Spinal Cord
The next level of localization to consider as we descend down the neuroaxis is the spinal cord. We previously covered the syndromes of the spinal cord in great detail.
But this is a good time to put all of those spinal cord syndromes into the context of the entire neuroaxis and attempt to differentiate them from neurologic deficit patterns that might occur above or below the level of the spinal cord.

54. Simplified spinal cord for clinical case analysis
Remember the long tracts that assist with understanding the localization of various spinal cord syndromes:
Descending: corticospinal tract
Ascending: Spinothalamic tract and dorsal columns.
The items I use almost as much for spinal cord are a knowledge of the autonomics:

55. Spinal cord syndromes Complete transverse lesion
Hemisection (Brown-Sequard)
Posterior column loss
Anterior spinal syndrome
Central cord syndrome
Here again we are not going to go through all of these spinal cord syndromes in detail. However, think about the primary feature of a spinal cord syndrome – there is a level! A motor level or a sensory level or both. Sometimes it is only a hemisensory level as in Brown-Sequard. Sometimes it only involves some but not all functions as in the anterior spinal syndrome. Review these syndromes in your head using our long tract paradigm.

56. Remember crossing of pain and temperature fibers in cord
Remember that the pain fibers of the spinothalamic tract cross at or within one or two levels of the level where the fibers entered the dorsal horn.
This is helpful for figuring out the Brown Sequard syndrome and central cord syndromes.

57. UMN vs LMN signs Upper motor neuron signs: Lower motor neuron signs:
Increased tone spasticity
Hyperreflexia
Extensor plantar response
Lower motor neuron signs:
Decreased tone
Hyporeflexia
Flexor plantar response
Muscle atrophy, fasciculations
The spinal cord is where the UMN completes its journey and the LMN takes over as we head down the neuroaxis. The spinal cord has both upper motor neurons (descending corticospinal tracts) and lower motor neurons (ventral horn motor cell bodies) in it. Sometimes there can be a mix of UMN and LMN signs in a spinal cord disorder although the UMN signs usually predominate!
You must get clear the neurologic examination findings that differentiate between UMN and LMN lesions.
It is easy –
Everything goes up in an UMN lesion – reflexes, tone, toes
Everything goes down in a LMN lesion – reflexes, tone, toes, and eventually muscle bulk.

58. Atrophy of Interossei muscles
Atrophy is more prominent with
weakness of LMN etiology
An example of atrophy to remind you that it is more prominent in a LMN lesion. This is a good clue for localization.
That does not mean that atrophy will not occur in an UMN syndrome/ lesion.
I have many patients with multiple sclerosis with paraplegia (UMN etiology) and they do develop significant leg muscle atrophy over time, but it will occur more quickly and more severely with a LMN syndrome.

59. Reflexes Myotatic stretch reflexes
Monosynaptic reflex: stretch muscle, stimulate Ia sensory afferent, stimulate alpha motorneuron
Ankle S1, S2
Patellar L3, L4
Biceps C5, C6
Triceps C7, C8
Reflexes are helpful to differentiate UMN from LMN weakness.
You should memorize these levels.

60. Reflex arc
This is just to remind you about the monosynaptic muscle stretch reflex.
Various descending inputs from cerebrum and brainstem help to modulate the reflex by providing suprasegmental input.
UMN lesions result in spasticity and hyperreflexia because of loss of supraspinal inhibitory input.

61. Stupid Neurology cartoon
Who could not like this? Come on, admit it. You smiled just a tiny bit…

62. Come back for Part 2 – It is much shorter!

63. Thank you for completing this module?
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64. Survey
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