Neuro ? Postmidterm

Front 1

28. Where does syringomyelia most frequently occur?

Back 1

28. Where does syringomyelia most frequently occur? In the cervical region

Front 2

29. Which direction does syringomyelia usually develop?

Back 2

29. Which direction does syringomyelia usually develop? Ventrally

Front 3

6. Broca’s area:
7. Wernike’s area:
8. Primary auditory cortex:
9. Primary motor cortex:
10. Primary somatosensory cortex:
11. Posterior parietal area:
12. Premotor cortex:
13. Are of brain that initiates voluntary horizontal eye movements:
14. Which areas are active in simple repeated finger flexion:

15. Which areas are active when performing complex finger movements:

16. Which areas are active in mental rehearsal of complex finger movements:

17. What areas receive input when movements are initiated by SENSORY stimuli:

18. What areas receive input when movements are initiated by EXTERNAL SENSORY events:

Back 3

6. Broca’s area: R & S [44, 45]
7. Wernike’s area: K [22]
8. Primary auditory cortex: P & Q [41 & 42]
9. Primary motor cortex: D [4]
10. Primary somatosensory cortex: A, B, C [3, 1, 2]
11. Posterior parietal area: E & G [5 & 7]
12. Premotor cortex: F [6]
13. Are of brain that initiates voluntary horizontal eye movements: H [8 Frontal eye field]
14. Which areas are active in simple repeated finger flexion: D [4 – Primary motor cortex moving the finger] & C, A, B [3, 1, 2 Primary somatosensory cortex indicating where finger is in space]
15. Which areas are active when performing complex finger movements: D [4 – Primary motor cortex moving the finger] & C, A, B [3, 1, 2 Primary somatosensory cortex indicating where finger is in space] & Medial part of F [Medial part of 6 – Called supplementary motor cortex used for the planning of complex movements]
16. Which areas are active in mental rehearsal of complex finger movements: Medial part of F [Medial part of 6 (premotor cortex) called supplementary motor cortex]
17. What areas receive input when movements are initiated by SENSORY stimuli: D [4 – Primary motor cortex] gets input from limb muscles they control via VPL of thalamus [body] or VPM of thalamus [face] or C, A, & B [3, 1, 2 – Primary somatosensory cortex]
18. What areas receive input when movements are initiated by EXTERNAL SENSORY events: F [LATERAL part of 6 (Premotor cortex)] gets input from C, A, & B [3, 1, 2 – Primary somatosensory cortex] & E & G [5 & 7 – Posterior parietal area]

Front 4

16. What is the difference between a myotonia & a myasthenia?

Back 4

Myotonias are defects of the muscle itself while myasthenia’s are defects of the synaptic cleft/end plate

Front 5

9. In basal ganglion regulation of movement the Ventral lateral thalamic nucleus releases the NT _______________ into the ____________________________________.

Back 5

9. In basal ganglion regulation of movement the Ventral lateral thalamic nucleus releases the NT _______________ into the ____________________________________.
Glutamate, Premotor area [Area 6] in the cortex

Front 6

30. This is a substance often found in synthetic narcotic drugs that can cause parkinsonism by damaging mitochondrial cells in the SNc:

Back 6

30. This is a substance often found in synthetic narcotic drugs that can cause parkinsonism by damaging mitochondrial cells in the SNc:
MPTP

Front 7

31. This is a D2 agonist:
32. This is a D1 & D2 agonist:

Back 7

31. This is a D2 agonist: BROMOCRIPTINE
32. This is a D1 & D2 agonist: PEROGLIDE

Front 8

47. 40yo patient enters your office. You notice dysmetria of legs, truncal ataxia, lurching gait, intention tremor of trunk and legs but NOT of their arms:

Back 8

47. 40yo patient enters your office. You notice dysmetria of legs, truncal ataxia, lurching gait, intention tremor of trunk and legs but NOT of their arms: D [Alcohol abuse, usually attributed to accompanying vitamin deficiency], Anterior Lobe & Some parts of Vermis [Degeneration of Purkinje cell’s. Nystagmus, dysarthria, & hypotonia NOT common]

Front 9

48. A 6yo boy enters your office with his mother. You notice a wide-based stance, truncal ataxia, hypotonia that is unequal, disorder of balance, nystagmus, headache, vomiting, & papilledema

Back 9

48. A 6yo boy enters your office with his mother. You notice a wide-based stance, truncal ataxia, hypotonia that is unequal, disorder of balance, nystagmus, headache, vomiting, & papilledema: A [Cerebellar tumor of midline astrocytoma causing increased ICP]

Front 10

49. 60yo patient comes into the ER due to the onset of some sudden symptoms. You notice truncal ataxia, intention tremor, limb dysmetria, dysdiadochokinisea, & rebound phenomenon on one side of their body:

Back 10

49. 60yo patient comes into the ER due to the onset of some sudden symptoms. You notice truncal ataxia, intention tremor, limb dysmetria, dysdiadochokinisea, & rebound phenomenon on one side of their body: B [Cerebellar stroke on ipsilateral side of symtpons]

Front 11

50. A 3yo is brought into your office b/c the parents have noticed delayed motor development, hasn’t been growing, gets sick very often. The child has ataxia, dysarthria, facial weakness, and difficulty generating horizontal saccades:

Back 11

50. A 3yo is brought into your office b/c the parents have noticed delayed motor development, hasn’t been growing, gets sick very often. The child has ataxia, dysarthria, facial weakness, and difficulty generating horizontal saccades: C [Louis-Bar syndrome] Autosomal recessive defect in chromosome 11, child will also have retarded sexual development

Front 12

51. Ataxia, Intention tremor, Ipsilateral hyptonia, Decomposition of movement, Ipsilateral dysdiadochokinesia, Ipsilateral dysmetria, Dysarthria:

52. Imbalance [falls to side of lesion], Gait ataxia, Dyssnergia:

53. Truncal ataxia, Wide-based stance, Inability to walk heel-to-toe, Nystagmus, Titubation, Head tilt:

Back 12

51. Ataxia, Intention tremor, Ipsilateral hyptonia, Decomposition of movement, Ipsilateral dysdiadochokinesia, Ipsilateral dysmetria, Dysarthria: Cerebro cerebellum [Lateral cerebral hemispheres]
52. Imbalance [falls to side of lesion], Gait ataxia, Dyssnergia: Spino-cerebellum [Dyssnergia = arm ataxia, Vermis & paravermis]
53. Truncal ataxia, Wide-based stance, Inability to walk heel-to-toe, Nystagmus, Titubation, Head tilt: Vestibulo-cerebellum [Floculus & nodulus]

Front 13

5. Where are the 3 levels of bladder control?

Back 13

5. Where are the 3 levels of bladder control?
Supratentorial level [Area 4 & hypothalamus]
Pontine micturition center [Posterior fossa]
Spinal cord [Sacral splanchnic: Parasympathetic & Pelvic splanchnic: Sympathetic]

Front 14

10. Which nucleus is responsible for receiving light input from the retina & maintaining the circadian clock?

Back 14

10. Which nucleus is responsible for receiving light input from the retina & maintaining the circadian clock?

SUPRACHIASMIC

Front 15

15. What are the 5 main structures in the limbic system:

Back 15

15. What are the 5 main structures in the limbic system: Cingulate gyrus, Isthmus, Parahippocampal gyrus, Uncus, Subcallosal gyrus

Front 16

23. Which structures receive information from the central nucleus in the conditioned fear response?

Back 16

23. Which structures receive information from the central nucleus in the conditioned fear response? G & F [Hypothalamus & Periaqueductal gray matter]

Front 17

24. Which structure initiates the autonomic response to a conditioned fear response?
25. Which structure initiates the emotional experience of a conditioned fear response?
26. Which structure initiates the behavioral reaction to a conditioned fear response?

Back 17

24. Which structure initiates the autonomic response to a conditioned fear response? G [Hypothalamus]
25. Which structure initiates the emotional experience of a conditioned fear response? I [Cerebral cortex]
26. Which structure initiates the behavioral reaction to a conditioned fear response?
PERIAQUEDUCTAL GRAY MATTER

Front 18

33. How will seizures originating in the temporal lobe present?

Back 18

33. How will seizures originating in the temporal lobe present?
Often start with olfactory or gustatory hallucinations [foul smell, metallic taste]
Often followed by mood change [feelings of anxiety or severe lonliness]
Lapse into a dreamy state
Motor phase that consists of coordinated complex behaviors
After seizure ends patient does not recall experience [memory function temporarily shut down]

Front 19

31. A tumor of the amygdala will probably affect behavior in what manner?


32. A tumor of the hypothalamus will probably affect behavior in what manner?

Back 19

31. A tumor of the amygdala will probably affect behavior in what manner? It will probably lead to extreme hostility & aggressive behavior.
32. A tumor of the hypothalamus will probably affect behavior in what manner? Often accompanied by spontaneous fits of anger or profound sadness

Front 20

10. Which motor tracts get direct input from the anterolateral system [spinothalamic tract]?

11. Which of the motor tracts in the previous questions gets the more powerful input from the ALS?

Back 20

10. Which motor tracts get direct input from the anterolateral system [spinothalamic tract]? Medullary [lateral] reticulospinal & Pontine [medial] reticulospinal
11. Which of the motor tracts in the previous questions gets the more powerful input from the ALS? Medullary [lateral] reticulospinal

Front 21

13. This nucleus releases SEROTONIN onto the substantia gelatinosa where it modulates transmission of PAIN information?

14. This nucleus releases SEROTONIN in many regions of the brain, in order to RAISE arousal levels as well as effect other aspects of behavior [e.g. mood]?
15. This nucleus releases ACh in many locations in the brain, in order to MAINTAIN arousal?
16. This nucleus releases ACh in many locations in the brain, in order to RAISE & MAINTAIN arousal?

17. This nucleus releases norE in many locations in the brain, in order to RAISE & MAINTAIN arousal?

18. This nucleus releases norE onto the substantia gelatinosa where it modulates transmission of PAIN information?
19. Besides the brain stem where else do neurons of the ARAS originate from?

Back 21

13. This nucleus releases SEROTONIN onto the substantia gelatinosa where it modulates transmission of PAIN information? B [Caudal raphe nuclei particularly magnus] → Think caudal → tail → works down in the body
14. This nucleus releases SEROTONIN in many regions of the brain, in order to RAISE arousal levels as well as effect other aspects of behavior [e.g. mood]? A [Rostral raphe nuclei] → Think rostral → head → works higher up in the brain
15. This nucleus releases ACh in many locations in the brain, in order to MAINTAIN arousal? E [Septal nuclei]
16. This nucleus releases ACh in many locations in the brain, in order to RAISE & MAINTAIN arousal? D [Basal nucleus of Meynert]
17. This nucleus releases norE in many locations in the brain, in order to RAISE & MAINTAIN arousal? C [Locus ceruleus]
18. This nucleus releases norE onto the substantia gelatinosa where it modulates transmission of PAIN information? C [Locus ceruleus]
19. Besides the brain stem where else do neurons of the ARAS originate? F [Basal forebrain]
Note: There are many nuclei in the raphe, some are caudal & some are rostral.

Front 22

20. How many branches does the ascending arousal system have?
21. Where do the branches synapse?

Back 22

20. How many branches does the ascending arousal system have? 2
21. Where do the branches synapse?
One synapses mainly on thalamic relay neurons
The other PENETRATES the lateral hypothalamus joins w/ other fibers to synapse everywhere in cortical regions

Front 23

Name of breathing - give lesion location

1. hyperventilation
2. ataxic
3. respiratory arrest
4. cheyne stokes
5. apneustic

Back 23

Name of breathing - give lesion location

1. hyperventilation - MIDBRAIN
2. ataxic - LOWER PONS, UPPER MEDULLA
3. respiratory arrest - MEDULLA BILATERAL
4. cheyne stokes - FOREBRAIN
5. apneustic - UPPER PONS

Front 24

51. In what part of the brain is the mesencephalic reticular formation located?
52. What does the mesencephalic reticular do?

Back 24

51. In what part of the brain is the mesencephalic reticular formation located? Midbrain
52. What does the mesencephalic reticular do? Organizes vertical eye movements

Front 25

possible lesion areas in a comatose patients.
53. Patient has gaze paralysis to the left:

Back 25

possible lesion areas in a comatose patients.
53. Patient has gaze paralysis to the left: Left pons [Left CN VI, Left PPRF lesion], Left Internal Capsule

Front 26

54. Both eyes deviated laterally w/ large unreactive pupils:LESION?

Back 26

54. Both eyes deviated laterally w/ large unreactive pupils: Midbrain [bi-lateral loss of CN III]

Front 27

17. What part of your brain is responsible for prosody?
18. Patient is unable to speak at all but is still able to sing & learn new songs. Where is the lesion?
19. This patient is no longer able to sign. Where is the lesion?
20. Where are broca’s & wernicke’s areas located?
21. 4% of humans use this hemisphere for language processing & grammar?

Back 27

17. What part of your brain is responsible for prosody? Right hemisphere [e.g. sarcasm, emotion]
18. Patient is unable to speak at all but is still able to sing & learn new songs. Where is the lesion? Left hemisphere
19. This patient is no longer able to sign. Where is the lesion? Left hemisphere
20. Where are broca’s & wernicke’s areas located? Left hemisphere
21. 4% of humans use this hemisphere for language processing & grammar? Right hemisphere [96% use left]

Front 28

60. Wernicke’s:
61. Transcortical sensory:
62. Gerstmann syndrome:
63. Conduction:

64. Broca’s:

65. Transcortical motor:
66. Global:
67. Alexia:

Back 28

60. Wernicke’s: Language fluent but meaningless [word-salad]
61. Transcortical sensory: Inability to speak spontaneously w/ the preservation of repetition & naming
62. Gerstmann syndrome: Inability to translate visual patterns into meaningful information
63. Conduction: Language areas are intact w/ connection between them severed. The patient can understand what is said but can’t repeat. When speaking the patient will make mistakes & realize them & attempt to correct them but continue making mistakes in the process.
64. Broca’s: Difficulty speaking & repeating words with intact comprehension. Patients speak in slow & simple sentences & become frustrated because their comprehension is intact.
65. Transcortical motor: Similar to Broca’s but less severe with the ability to repeat long sentences
66. Global: Unable to comprehend or produce language
67. Alexia: Patients are unable to read from the left visual field b/c of a disconnect between the hemispheres

Front 29

69. Besides reading difficulties what other problems might dyslexic patients have?


70. Why do dyslexic patients have the problem in the previous question?

Back 29

69. Besides reading difficulties what other problems might dyslexic patients have? The inability to process transient sensory input quickly. Rapid conduction in the visual system is below average.
70. Why do dyslexic patients have the problem in the previous question? Cells in the magnocellular layers of the LGN are smaller than normal [depth & motion & they radiate parietally]. Remember parvocellular cells radiate temporally [form & color]

Front 30

5. What are the three major classes of symptoms in schizophrenia & the presence of which type of symptom indicates the poorest prognosis?




6. What types of hallucinations are most common in schizophrenics?

Back 30

5. What are the three major classes of symptoms in schizophrenia & the presence of which type of symptom indicates the poorest prognosis?
Positive symptoms: Additional pathological symptoms
Negative symptoms: Loss of function [presence indicates poorer prognosis]
Disorganized symptoms: Disorder of thought & memory dysfunction & confusion
6. What types of hallucinations are most common in schizophrenics? Auditory [sometimes visual, olfactory, gustatory, or tactile] → They can relate unusually meaning or significance to normal events

Front 31

7. What are the prodromal signs of a psychotic episode?

Back 31

7. What are the prodromal signs of a psychotic episode? Social isolation & withdrawal, Impairment in normal fulfillment of expected roles, Odd behavior & ideas, Neglect of personal hygiene, Flat affect

Front 32

13. What are the anatomical anomalies commonly seen in schizophrenics?

Back 32

13. What are the anatomical anomalies commonly seen in schizophrenics?
Reduced blood flow to left globus pallidus: Disturbance is system connecting basal ganglia to frontal lobes
Blood flow does not increase in frontal lobes during tests of working memory:
Cortex of medial temporal lobe is thinner & the anterior portion of the hippocampus is smaller than in normal people: Hippocampal likely the cause of memory defects
Lateral & 3rd Ventricles are enlarged:
Wider sulci:
Reduced volume of temporal & frontal lobes:

Front 33

36. What are the anatomical changes that occur in bipolar patients during their manic & depressive episodes?
Depressive phase: Reduced activity in area of prefrontal cortex below the genu of the corpus callosum
Manic phase: Increased activity in area of prefrontal cortex below the genu of the corpus callosum
This subgenul region is important for mood states & has connections w/ other regions involved in emotion [amygdala, lateral hypothalamus, nucleus accumbens, NorE, serotnergic, dopaminergic systems of the brain]

Back 33

36. What are the anatomical changes that occur in bipolar patients during their manic & depressive episodes?

Front 34

9. People that are genetically prone to addiction have what difference in NT activity compared w/ people that don’t?

Back 34

9. People that are genetically prone to addiction have what difference in NT activity compared w/ people that don’t?
REDUCTION IN 5-HT (SEROTONIN)

Front 35

12. According to Cloniger what are the 3 personality factors that are important in developing addiction?

Back 35

12. According to Cloniger what are the 3 personality factors that are important in developing addiction?

Novelty seeking, Harm avoidance, Reward dependence

Front 36

13. How did Cloniger describe his two “types” of addiction?

Back 36

13. How did Cloniger describe his two “types” of addiction?

Type 1: Low novelty seeking, High harm avoidance, High reward dependence
Type 2: High novelty seeking, Low harm avoidance, Low reward dependence

Front 37

34. What change in what NT results in the symptoms of hyperhidrosis, tachycardia, hypertension, & tremor in alcohol withdrawal?

35. What change in what NT results in psychotic symptoms in alcohol withdrawal?

36. What change in what NT results in epileptic seizures in alcohol withdrawal?

Back 37

34. What change in what NT results in the symptoms of hyperhidrosis, tachycardia, hypertension, & tremor in alcohol withdrawal? Increased NorE

35. What change in what NT results in psychotic symptoms in alcohol withdrawal? Increased dopamine

36. What change in what NT results in epileptic seizures in alcohol withdrawal? Increased glutamate

Front 38

44. What drug is used most often in the treatment of alcohol withdrawal?

Back 38

44. What drug is used most often in the treatment of alcohol withdrawal? Benzodiazapenes

Front 39

Which of the following are anti-convulsive, anti-adrenergic, anti-psychotic

diazapam
clinidine
holoperidol

Back 39

anti-convulsive - diazapam
anti-psychotic - haloperidol
anti-adrenergic - clonidine

Front 40

what medication is used for warm opiate detox?

hyposomnia with warm or cold?

Back 40

methadone

hyposomnia with COLD

Front 41

2. What is rhabdomyolysis?

5. What are EEG’s used to assess?

Back 41

2. What is rhabdomyolysis? Rapid breakdown/death of skeletal muscle

5. What are EEG’s used to assess? Brain death, Brain damage, epilepsy, sleep

Front 42

9. Sharp waves, spikes, & spike waves in an EEG are called what?

10. When your waves have a lower frequency than they should they are known as?

Back 42

9. Sharp waves, spikes, & spike waves in an EEG are called what? Epileptiform activity
10. When your waves have a lower frequency than they should they are known as? Slow waves [the slower the wave the more severe the abnormality]

Front 43

12. Seizures can be classified into 2 general categories. What are they?

Back 43

12. Seizures can be classified into 2 general categories. What are they?
Primary seizures: Cause is unknown [idiopathic], Individuals simply have a reduced threshold for seizues
Secondary seizures: Result from KNOWN pathological lesion or disease process & can be split into 2 subcategories
(1) Focal: From a focal lesion
(2) Generalized: Diffuse process causing widespread disturbance of brain function

Front 44

13. Give some examples of intracranial causes of seizure:

14. Give some examples of extracranial causes of seizure:

Back 44

13. Give some examples of intracranial causes of seizure: Tumor, CVA, Trauma, Brain infection, Congential [e.g tuberosclerosis → causes benign tumors to grown in all body organs]
14. Give some examples of extracranial causes of seizure: Metabolic [e.g. electrolyte, biochemical], Anoxia, Hypoxia, Drugs, Withdrawal

Front 45

18. What component of bacterial cell walls induces sleep?

19. What cytokine is most commonly associated w/ inducing NREM sleep?

20. Which substance acts as a inhibits the ARAS at it’s highest concentration by acting as a modulator at synapses?

21. What are the strongest candidates for humoral agents that induce sleep?

Back 45

18. What component of bacterial cell walls induces sleep? Muramyl peptides

19. What cytokine is most commonly associated w/ inducing NREM sleep? IL-1

20. Which substance acts as a inhibits the ARAS at it’s highest concentration by acting as a modulator at synapses? Adenosine

21. What are the strongest candidates for humoral agents that induce sleep? Melatonin & Adenosine

Front 46

33. What causes the K-complex?

34. Which causes sleep spindles?

35. The characteristic δ waves of NREM 4 are caused by?

Back 46

33. What causes the K-complex? Synchronized firing of cortical neurons
34. Which causes sleep spindles? Rhythmic firing of thalamocortical neurons [associated w/ diminished sensory input to cortex]
35. The characteristic δ waves of NREM 4 are caused by? Characteristic inherent synchronous firing of cortical neurons largely relieved of sensory input from the thalamus and input from the ARAS.

Front 47

36. What immediately precedes the onset of REM sleep?

37. What part of the thalamus is most active during REM sleep?

Back 47

36. What immediately precedes the onset of REM sleep? PGO [pontine-geniculo-occipital] wave which is the firing of some cholinergic neurons of the ARAS that raise the excitability of the thalamus
37. What part of the thalamus is most active during REM sleep? LGN [stands to reason the visual cortex will be the most active cortex]

Front 48

39. What causes the paralysis characteristic of REM sleep?

Back 48

39. What causes the paralysis characteristic of REM sleep? Activation of lateral [medullary] reticulospinal tract [remember it is glycinergic so it is inhibitory]

Front 49

40. Which neurons in the ARAS are firing the most during REM sleep?

Back 49

40. Which neurons in the ARAS are firing the most during REM sleep? ↑Firing of cholinergic [septal nuclei & basal nucleus of meynert] & ↓firing of locus ceruleus & rostral raphe nuclei [NorE & Serotonin respectively]

Front 50

30. What are the morphological changes that occur in LTP?

31. How do these morphological changes come about?

Back 50

30. What are the morphological changes that occur in LTP?
1st early effects: Increase in AMPA channel conductions & Increase in AMPA channel #
2nd late effects: Formation of new dendritic spines → increase in # of synapses

31. How do these morphological changes come about?
1st Glutamate opens AMPA channels → Depolarization due to Na+ entry
2nd Continuous depolarization removes Mg2+ from NMDA channels → Ca2+ entry
3rd Ca2+ activates protein kinase C & calcium-calmodulin dependant kinase II [CAMKII]

Front 51

32. What stimulation frequency is required to induce LTD in CA1 Neurons:

33. What are the morphological changes that occur in LTD?

34. How do these morphological changes come about?

Back 51

32. What stimulation frequency is required to induce LTD in CA1 Neurons: About 1/s

33. What are the morphological changes that occur in LTD? Internalization of AMPA channels

34. How do these morphological changes come about? Activation of protein phosphotases → Dephosphorylation of AMPA channels → AMPA channel internalization

Front 52

35. What channel must be activated in both LTP & LTD?

Back 52

35. What channel must be activated in both LTP & LTD? NMDA, the key difference being the AMOUNT of Ca2+ entering

Front 53

36. What are the 3 major sites for procedural memory?

38. What are the only output cells of the cerebellar cortex?

39. What are the major excitatory inputs to the output cells of the cerebellar cortex?

Back 53

36. What are the 3 major sites for procedural memory? Supplementary & premotor cortex [Area 6], Striatum [Caudate+Putamen], Cerebellum

38. What are the only output cells of the cerebellar cortex? Purkinje cells
39. What are the major excitatory inputs to the output cells of the cerebellar cortex?
Climbing fibers: From inferior olivary nucleus, Each has several hundred synapses on purkinje cells
Mossy/Parallel fibers [molecular layer]: Information from all other inputs, Each has a single synapse on purkinje cells

Front 54

42. What three things have to happen for LTD of purkinje cells?

Back 54

42. What three things have to happen for LTD of purkinje cells? These must happen simultaneously
Rise in intracellular Ca2+ by climbing fiber stimulation
Rise in intracellular Na+ from AMPA channel opening [parallel fiber]
Activation of protein kinase C from glutamate metabotropic receptor activation [parallel fiber]

Front 55

44. What is Korsakoff’s syndrome?

Symptoms? Acute and Chronic?

Back 55

44. What is Korsakoff’s syndrome?
Cause: Vitamin B1 (Thiamin) deficiency due to malnutrition, generally as a result of alcoholism resulting in bilateral loss of cells in dorsomedial thalamus & mammilary bodies
Symptoms:
(1) Acute phase [Wernike]: Confusion, Confabulation, Stupor, Ataxia
(2) Chronic phase [Korsakoff]: Memory impairment, may show anterograde amnesia [probably b/c of damage to thalamus & hippocampus] & severe retrograde amnesia

Front 56

2. What is the most common cause of dementia?

10. What are the 3 cardinal signs of Alzheimer’s disease?

Back 56

2. What is the most common cause of dementia? Alzheimer’s disease

10. What are the 3 cardinal signs of Alzheimer’s disease?
Neuritic senile plaques: EXTRACELLULAR deposits that are roughly spherical [200nm in diameter] containing neuronal processes
Neurofibrillary tangles: INTRACELLULAR paired helical filaments [10nm in diameter]
Granulovacuolar degeneration: INTRACELLULAR circular clear zones of cytoplasm

Front 57

11. Where is the loss of neurons most notable in Alzheimer’s disease?

12. Neurons secreting what types of NT’s are most affected?

Back 57

11. Where is the loss of neurons most notable in Alzheimer’s disease? Hippocampus, Entorhinal cortex, Association cortices, Basal nucleus of Meynert
12. Neurons secreting what types of NT’s are most affected? NorE, ACh, Dopamine

Front 58

16. What occurs in Alzheimer’s disease that results in the protein forming plaques?

17. What is the proposed mechanism of the formation of neurofibrillary tangles?

Back 58

16. What occurs in Alzheimer’s disease that results in the protein forming plaques?
Normally: Precursor protein is cleaved by α-secretases & part of the APP is released into the ECF
Alzheimer’s: Precursor proteins are cleaved by β/γ-secretases into a smaller peptide → Formation of plaques
17. What is the proposed mechanism of the formation of neurofibrillary tangles? Toxic external plaques induce damage in the neurons causing the tangles

Front 59

18. What proteins form the neurofibrillary tangles?

19. What is the function of these proteins normally?

20. What change occurs to these proteins to induce the formation of neurofibrillary tangles?

Back 59

18. What proteins form the neurofibrillary tangles? τ proteins
19. What is the function of these proteins normally? Bind to microtubules during assembly-disassembly cycles & promote assembly and stability

20. What change occurs to these proteins to induce the formation of neurofibrillary tangles?
HYPERPHOSPHORYLATION

Front 60

29. What are the histological signs of Friedreich’s ataxia?

30. When is the typical onset of Friedreich’s ataxia?

Back 60

29. What are the histological signs of Friedreich’s ataxia? Atrophy of the dorsal columns, corticospinal tracts, & spino-cerebellar tracts
30. When is the typical onset of Friedreich’s ataxia? 1st or 2nd decade

Front 61

36. What are the signs & symptoms of Pick’s Disease?

37. When is the usual onset of this disease?

38. What population is most at risk?
39. What types of neurons are most affected?

40. What are the histological signs?

Back 61

36. What are the signs & symptoms of Pick’s Disease? A form of dementia that leads to death within 10 years & also presents w/ behavioral disturbances & aphasia

37. When is the usual onset of this disease? 4th or 5th decade

38. What population is most at risk? Women

39. What types of neurons are most affected? Cholinergic [especially in basal nucleus of Meynert]

40. What are the histological signs? Cortical atrophy [usually unilateral & localized in frontal or temporal lobe]. Neurons contain cytoplasmic inclusions known as Pick bodies [made of densely packed neurofilament].

Front 62

49. What is the name of the disease that is characterized by rapid aging in children?
50. What is the cause of the disease in the previous question?


51. When does this disease become evident?
52. When is this disease usually result in death?

Back 62

49. What is the name of the disease that is characterized by rapid aging in children? Progeria

50. What is the cause of the disease in the previous question? Gene mutation in a protein that normally holds the nucleus and the cell togther

51. When does this disease become evident? 2 years after birth

52. When is this disease usually result in death? Anywhere between 8-21 years due to heart disease

Front 63

19. Internuclear opthalmoplegia is due to a lesion in the?
20. Binuclear opthalmoplegia is due to a lesion in the?
21. If a patient has a lesion of their right MLF how will they present?

22. If a patient has a lesion of both MLFs how will they present?

Back 63

19. Internuclear opthalmoplegia is due to a lesion in the? MLF on one side
20. Binuclear opthalmoplegia is due to a lesion in the? MLF on both sides
21. If a patient has a lesion of their right MLF how will they present? On gaze to the left the right eye will not adduct and the eye on the left will exhibit nystagmus
22. If a patient has a lesion of both MLFs how will they present? On gaze in either direction they eye that is supposed to adduct won’t and the abducted eye will exhibit nystagmus

Front 64

converge
24. A patient has an intact pupillary reflex but has both their eyes deviated to the right. They have no other neurological deficits. Where might the lesion be?

25. A patient has an intact pupillary reflex but has both eyes deviated to the left. On leftward gaze the left eye exhibits nystagmus & the right eye does not adduct? Where might the lesion be?

Back 64

converge
24. A patient has an intact pupillary reflex but has both their eyes deviated to the right. They have no other neurological deficits. Where might the lesion be? Left PPRF

25. A patient has an intact pupillary reflex but has both eyes deviated to the left. On leftward gaze the left eye exhibits nystagmus & the right eye does not adduct? Where might the lesion be? Right PPRF & Right MLF

Front 65

26. A patient has an intact pupillary reflex but has both their eyes deviated to the right. Their tongue deviates to the left on protrusion. Where might the lesion be? What other symptoms might you see?

Back 65

26. A patient has an intact pupillary reflex but has both their eyes deviated to the right. Their tongue deviates to the left on protrusion. Where might the lesion be? What other symptoms might you see? Right Internal Capsule, Loss of sensation & UMN syndrome on the side contralateral to the lesion, Patient will have UMN of muscles of facial expression in lower face on contralateral side but will still be able to wrinkle their forward on the side contralateral to the lesion

Front 66

what is it?
Contralateral:
chorea
tremor
sensory loss
paresis

Back 66

what is it?
Contralateral:
chorea
tremor
sensory loss
paresis

BENEDIKT SYNDROME - midbrain PCA
red nucleus, substantia nigra, medial lemniscus, and crus cerebri (with motor tracts) affected

Front 67

what is it?
Ipsi: deviation of eye, opthalmoplegia
contra: paresis, parkinsons, deviation of tongue, lower facial paralysis

Back 67

what is it?
Ipsi: deviation of eye, opthalmoplegia
contra: paresis, parkinsons, deviation of tongue, lower facial paralysis

WEBER SYNDROME -Midbrain Basilar Artery:
Corticobulbar, Corticospinal and Substantia nigra affected

Front 68

what is it?
bilateral paralysis only vertical eye movements

Back 68

bilateral paralysis - Pons - Basilar branches
MLF saved

Front 69

what is it?
contralateral anesthesia
ipsislateral facial anesthesia, horners
vertigo
nystagmus
dysphagia.dysarthia

Back 69

what is it?
contralateral anesthesia
ipsislateral facial anesthesia, horners
vertigo
nystagmus
dysphagia.dysarthia

WALLENBERG (LATERAL MEDULLARY SYNDROME)
-ALS, CN V, medial vestibular nuclei, nucleus ambiguous

Front 70

What is it?
contralateral paresis, somatosensory loss
ipsilateral weakness of tongue,

Back 70

What is it?
contralateral paresis, somatosensory loss
ipsilateral weakness of tongue,
ANT SPINAL (MEDIAL MEDULLARY SYNDROME)
-ML , Corticospinal, hypoglossal nerve affected