Pbl Exam 3 Case 5

Front 1

1. Development of the neural tube

Back 1

During embryological development, the CNS arises from a sheet of ectodermal cells that folds over to form the neural tube.

The neural tube forms several swellings and outpouchings in the head that eventually develop into the brain, while the part of the neural tube running down the back fo the embryo forms the spinal cord.

The fluid filled cavities within the neural tube develop into the brain ventricles, which contain CSF.

Front 2

2. Three main divisions of the developing brain

Back 2

1. Prosencephalon (forebrain)
2. Mesencephalon (midbrain)
3. Rhombencephalon (hindbrain)

Front 3

3. Components of the prosencephalon

Back 3

1. Telencephalon
-Cerebral hemispheres
-Cerebral cortex
-Subcortical white matter
-Basal ganglia
-Basal forebrain nuclei

2. Diencephalon
-Thalamus
-Hypothalamus
-Epithalamus

Front 4

4. Components of the mesencephalon

Back 4

1. Cerebral peduncles
2. Midbrain tectum
3. Midbrain tegmentum

Front 5

5. Components of the rhombencephalon

Back 5

1. Metencephalon
-Pons
-Cerebellum

2. Myelencephalon
-Medulla

Front 6

6. Brainstem

What structures compose the brainstem?

Back 6

Most evolutionary ancient part of the human brain and is the part that most closely resembles the brains of fish and reptiles.

It controls many of the most basic bodily functions necessary for survival, such as respiration, blood pressure and heart rate.

Composed of :
1. Midbrain
2. Pons
3. Medulla

Front 7

7. CSF

Back 7

Formed mainly by vascular tufts lying within the ventricles called choroid plexus.

CSF circulates from the lateral ventricles to the third ventricle, and then leaves the ventricular system via foramina in the fourth ventricle, to percolate around the outside surface of the brain and spinal cord.

Front 8

8. Protective layers of the CNS

Back 8

The CNS is convered by three membranous protective layers called meninges.

Listed from inside to outside, the layers are the pia, arachnoid, and dura mater.

Once it leaves the ventricular system, CSF travels in the space between the arachnoid and pia and is ultimately reabsorbed into the venous system.

Front 9

9. Terms of orientation above the midbrain

Back 9

Anterior = rostral
Posterior = caudal
Superior = dorsal
Inferior = ventral

Front 10

10. Terms of orientation below the midbrain

Back 10

Anterior = ventral
Posterior = dorsal
Superior = rostral
Inferior = caudal

Front 11

11. Neurons

Back 11

Neurons are mainly responsible for signaling in the nervous system, although glial cells may contribute as well.

Typical neuron has a cell body containing the nucleus, relatively short processes called dendrites, which receive most inputs to the cell, and long processes called axons, which carry most outputs.

Front 12

12. Most mammalian neurons are of which type...?

Back 12

Most mammalian neurons are multipolar, meaning that they have several dendrites, as well as several axons.

Often, a single axon arising from the cell body will travel for a distance, and then one or several axon collaterals branch off the main axon to reach different targets.

Front 13

13. Bipolar neurons

Back 13

Some neurons are bipolar, with a single dendrite and a single axon arising from the cell body.

Bipolar cells are often sensory neurons, such as those involved in vision or olfaction.

Some bipolar neurons are also called pseudounipolar, since their processes are initially fused, and then split to produce two long axons.

An example is dorsal root ganglion sensory neurons.

Front 14

14. Unipolar neurons

Back 14

Unipolar neurons, in which both axons and dendrites arise from a single process coming off the cell body, occur mainly in invertebrates.

Front 15

15. What are the two general functions of chemical neurotransmitters?

Back 15

1. Mediate rapid communication between neurons thru EPSPs and IPSPs.

2. Neuromodulation

Front 16

16. Neuromodulation

Back 16

Generally occurs over slower time scales than IPSPs and EPSPs

Includes a broad range of cellular mechanisms involving signaling cascades that regulate synaptic transmission, neuronal growth, and other functions.

Neuromodulation can either facilitate or inhibit the subsequent signaling properties of the neuron.

Front 17

17. Gray matter vs. white matter

Back 17

Areas of the CNS made up mainly of myelinated axons are called white matter; areas made up mainly of cell bodies are called gray matter.

Most of the local synaptic communication between neurons int he CNS occurs in the gray matter, while axons in the white matter transmit signals overs greater distances.

Front 18

18. Cerebral cortex

What lies beneath the cerebral cortex?

Back 18

The surface of the cerebral hemispheres is covered by a unique mantle of gray matter called the cerebral cortex, which is far more developed in higher mammals than in other species.

White matter lies beneath, which conveys signals to and from the cortex.

Front 19

19. Where else is gray matter found?

Back 19

Also found in large clusters of cells called nuclei located deep within the cerebral hemispheres and brainstem.

Examples include the basal ganglia, thalamus, and cranial nerve nuclei.

Front 20

20. Distribution of white and gray matter in the cerebral hemispheres, spinal cord, and brainstem

Back 20

In the cerebral hemispheres the gray matter cortex is outside, while the white matter is inside.

In the spinal cord the opposite is true: white matter pathways lie on the outside, while the gray matter is in the center.

In the brainstem, gray matter and white matter regions are found both on the inside and on the outside, although most of the outside surface is white matter.

Front 21

21. What are the different names for white matter pathways in the CNS?

Back 21

1. Tract
2. Fascicle
3. Lemniscus
4. Bundle

Front 22

22. Comissures

Back 22

A white matter pathway that connects identical structures on the right and left sides of the CNS is called a comissure.

Front 23

23. What controls the sympathetic and parasympathetic pathways?

Back 23

Controlled by higher centers in the hypothalamus and limbic system, as well as by afferent sensory information from the periphery.

Front 24

24. Sulci and gyri

Back 24

Sulci: numerous infoldings or crevices

Gyri: bumps or ridges of cortex that rise up between the sulci

Front 25

25. What separates the frontal lobes from the parietal lobes?

Back 25

The central sulcus (of Rolando)

Front 26

26. What separates the frontal lobes from the temporal lobes?

Back 26

An especially deep sulcus called the Sylvian fissure, or lateral fissure

Front 27

27. What separates the parietal lobes from the occipital lobes?

Back 27

The parieto-occipital sulcus

Front 28

28. What additional region of cerebral cortex lies buried within the depths of the Sylvian fissure?

Back 28

The insular cortex.

The insula is covered by a lip of frontal cortex anteriorly and parietal cortex posteriorly, called the frontal operculum and parietal operculum, respectively.

Front 29

29. What separates the two cerebral hemispheres?

Back 29

The interhemispheric fissure, AKA the longitudinal fissure.

A large C-shaped band of white matter called the corpus callosum connects homologous areas in the two hemispheres.

Front 30

30. What gyrus runs in front of the central sulcus?

What divides the remainder of the lateral frontal surface?

Back 30

The precentral gyrus

The remainder of the lateral frontal surface is divided into the superior, middle, and inferior frontal gyri by the superior and inferior frontal sulci.

Front 31

31. Divisions of the lateral temporal lobe

Back 31

The lateral temporal lobe is divided into superior, middle and inferior temporal gyri by the superior and middle sulci.

The most anterior portion of the parietal lobe is the postcentral gyrus, lying just behind the central sulcus.

The intraparietal sulcus divides the superior parietal lobule from the inferior parietal lobule.

Front 32

32. Divisions of the corpus callosum

What surrounds the corpus callosum?

Back 32

Consists of the rostru, genu, body, and splenium.

The cingulate gyrus surrounds the corpus callosum, running from the paraterminal gyrus anteriorly to the isthmus posteriorly

Front 33

33. Marginal branch of the cingulate gyrus

Back 33

This runs up to the superior surface and forms and important landmark, since the sulcus immediately in front of it on the superior surface is the central sulcus.

Front 34

34. Where does the primary motor cortex lie?

Back 34

Lies in the precentral gyrus int he frontal lobe.

This area controls movement of the opposite side of the body

Front 35

35. Where does the pimary somatosensory cortex lie?

Back 35

In the postcentral gyrus in the parietal lobe and is involved in sensation for the opposite side of the body.

Front 36

36. Where is the primary visual cortex located?

Back 36

In the occipital lobes along the banks of a deep sulcus called the calcarine fissure.

Front 37

37. Where is the primary auditory cortex located?

Back 37

Composed of the transverse gyri of Heschl, which are two finger-like gyri that lie inside the Sylvian fissure on the superior surface of each temporal lobe.

Front 38

38. Layers of the cerebral cortex

Where do they project their signals?

Back 38

Six cell layers:

Layer 1: Consists mainly of dendrites of neurons from deeper layers and axons
Layers 2 & 3: Contain neurons that project mainly to other areas of the cortex
Layer 4: Receives the majority of inputs from the thalamus
Layer 5: Projects mostly to subcortical structures other than the thalamus, such as the brainstem, spinal cord, and basal ganglia
Layer 6: Projects primarily to the thalamus.

Front 39

39. Thickness of the cortical cell layers

Back 39

Varies according to the main function of that area of cortex.

For example, the primary motor cortex has large efferent projections tot he brainstem and spinal cord, which control movement. It receives relatively little direct sensory information from thalamic relay centers. Therefore, in the primary motor cortex, Layer 5 is thicker and has more cell bodies than layer 4.

The opposite holds for primary visual cortex, where layer 4 contains many cell bodies and layer 5 is relatively cell poor.

Front 40

40. What is the most important motor pathway in humans?

Back 40

The corticospinal tract.

Begins mainly in the primary motor cortex, where neuron cell bodies project via axons down thru the cerebral white matter and brainstem to reach the spinal cord.

Front 41

41. Pyramidal decussation

Back 41

This crossing over occurs at the junction between the medulla and the spinal cord.

Front 42

42. Lesions above the pyramidal decussation produce...

Back 42

Contralateral weakness w/respect to the lesion

Front 43

43. Lesions below the pyramidal decussation produce...

Back 43

Ipsilateral weakness

Front 44

44. Upper motor neurons

Back 44

Motor neurons that project from the cortex down to the spinal cord or brainstem are referred to as upper motor neurons.

They then form synapses onto the lower motor neurons

Front 45

45. Lower motor neurons

Back 45

Located int he anterior horns of the central gray matter of the spinal cord or in brainstem motor nuclei.

The axons of LMNs project out of the CNS via the anterior spinal roots or via the cranial nerves to finally reach muscle cells in the periphery.

Front 46

46. Lesions in the cerebellum lead to...?

Back 46

Disorders in coordination and balance, often referred to as ataxia.

Front 47

47. Lesions in the basal ganglia cause...?

Back 47

Hypokinetic movement disorders, such as Parkinsonism, in which movements are infrequent, slow, and rigid, and hyperkinetic movement disorders, such as Huntington's disease, which is characterized by dancelike involuntary movements.

Front 48

48. Somatic sensation

Back 48

Somatic sensation refers to the conscious perceptions of touch, pain, temperature, vibration, and proprioception (lib or joint position sense).

Front 49

49. Somatosensory systems

What are the two main pathways?

Back 49

1. The posterior column pathways
2. Anterolateral pathways

Front 50

50. Posterior column pathways

Back 50

Conveys proprioception, vibration sense and fine, discriminative touch.

Primary sensory neuron axons first enter the spinal cord via the dorsal roots and then the ipsilateral white matter dorsal columns to ascend all the way to the dorsal column nuclei in the medulla.

It is here that they make synapses onto the secondary sensory neurons, which send out axons that cross over to the other side of the medulla. These axons continue to ascend, now on the contralateral side, and synapse in the thalmus, and from there neurons project to the primary somatosensory cortex in the postcentral gyrus.

Front 51

51. Anterolateral pathways

Back 51

Conveys pain, temperature sense, and crude touch.

Pimary sensory neurons also enter the spinal cord via the dorsal roots. However, these axons make their first synapses immediately in the gray matter of the spinal cord.

Axons from the secondary sensory neurons cross over to the other side of the spinal cord and ascend in the anterolateral white matter, forming the spinathalamic tract.

After synapsing in the thalamus, the pathway again continues to the primary somatosensory cortex.

Front 52

52. Thalamus

Back 52

Important relay center.

Nearly all pathways that project to the cerebral cortex do so after synapsing in the thalamus. The thalami are gray matter structures located deep within the cerebral white matter just above the brainstem and behind the basal ganglia.

They are shaped somewhat like eggs, with their posterior ends angled outward, together forming an inverted V in horizontal sections.

Front 53

53. Thalamus, sensory and nonsensory pathways

Back 53

The thalamus consists of multiple nucleu; each sensory modality has a different nuclear area where synapses occur before the information is related to the cortex (except for olfaction).

Nonsensory pathways also relay in the thalamus.

Front 54

54. Important feature of thalamic circuits

Back 54

The recipricoal nature of cortical thalamic connections.

Thus, virtually all cortical regions project strongly via layer 6 back to the thalamic areas from which their major inputs arise.

Front 55

55. Monosynaptic stretch reflex

Back 55

Well studied reflex arc that provides rapid local feedback for motor control.

Muscle spindles convey stretch rate in muscles to the distal processes of sensory neurons and is then conveyed via the dorsal roots into the spinal gray matter.

In the spinal gray matter the sensory neurons form multiple synapses, including some direct synapses onto LMNs in the anterior horn. The LMNs project via the ventral roots back out to the muscle, causing it to contract.

Tested via the reflex hammer, AKA DTR

Front 56

56. Reticular formation

Back 56

Extends throughout the central portions of the brainstem from the medulla to the midbrain.

The more caudal portions of the reticular formation in the medulla and lower pons tend to be involved mainly in motor and autonomic functions.

The rostral reticular formation in the upper pons and midbrain plays an imortant role in regulating the level of consciousness, influencing higher areas mainly through modculation of thalamic activity.

Thus, lesions that affect the pontomesencephalic reticular formation can cause lethargy and coma.

Front 57

57. What other forebrain networks are also important in maintaining consciousness?

Back 57

Cortical, thalamic, and other forebrain networks.

Therefore, the level of consciousness can also be impaired in bilateral lesions of the thalami or in bilateral lesions of the cerebral hemispheres.

Note that mass lesions above the brainstem often cause impaired consciousness indirectly when they exert pressure on the brainstem thru mass effect, thus distorting or compressing the reticular formation.

Front 58

58. Limbic system

Back 58

Located near the medial edge or fringe of the cerebral cortex.

Functions in olfaction, regulation of emotions, memory, appetitive drives, and autonomic and neuroendocrine control.

Front 59

59. What areas/structures are included in the limbic system?

Back 59

1. Certain cortical areas in the medial and anterior temporal lobes
2. Anterior insula
3. Inferior medial frontal lobes
4. Cingulate gyri
5. Hippocampal formation
6. Amygdala
7. Several nuclei in the medial thalmus, hypothalamus, basal ganglia, septal area, and brainstem

Front 60

60. Fornix

Back 60

A paired, arch-shaped white matter structure that connects the hippocampal formation to the hypothalamus and septal nuclei

Front 61

61. Lesions in the limbic system

Back 61

Cause deficits in the consolidation of immediate recall into longer-term memories.

In addition, they can cause behavioral changes and may underlie a number of psychiatric disorders.

Finally, epileptic seizures most commonly arise from the limbic structures of the medial temporal lobe, resulting in seizures that may begin w/emotions such as fear, memory distortions such as deja vu, or olfactory hallucinations.

Front 62

62. Association cortex

Back 62

Carries out higher-order information processing.

Front 63

63. Unimodal association cortex

Back 63

In unimodal association cortex, higher-order processing takes place mostly for a single sensory or motor modality.

Unimodal association cortex is usually located adjacent to a primary motor or sensory area; for example, unimodal visual association cortex is located adjacent to the primary visual cortex.

Front 64

64. Heteromodal association cortex

Back 64

Involved in integrating functions from multiple sensory and/or motor modalities.

Front 65

65. Language perception (what areas perceive it first?)

Back 65

Perceived first by the primary auditory cortex in the superior temporal lobe when listening to speech or by the primary visual cortex in the occipital lobes when we are reading.

Front 66

66. Wernicke's area

Back 66

Next, the cortical-cortical association fibers convey info to Wernicke's area in the dominant (usually left) hemisphere.

Lesions in this area cause deficits in language comprehension, also sometimes called receptive or sensory aphasia, or Wernicke's aphasia.

Front 67

67. Broca's area

Back 67

Located in the frontal lobe, also int he left hemisphere, adjacent to the areas of primary motor cortex involved in moving the lips, tongue, face, and larynx.

Lesions in this area cause deficits in the production of language, with relative sparing of language comprehension.

This is called expressive or motor aphasia, or Broca's aphasia

Front 68

68. Gerstmann's syndrome

Back 68

Lesions in the inferior parietal lobule in the left hemisphere produce difficulties with calculations, right-left confusion, inability to identify fingers by name (finger agosia), and difficulties with written language

Front 69

69. Apraxia

Back 69

Diffuse lesions of the cortex, or sometimes more focal lesions affecting the frontal or left parietal lobe, can produce abnormalities in motor conceptualization, planning, and execution, called apraxia.

Front 70

70. Parietal lobes and spatial awareness

Back 70

The parietal lobes also play an important role in spatial awareness. Thus, lesions here, especially in the nondominant hemisphere often cause a distortion or perceived space and neglect of the contralateral side.

For example, right parietal lesions can cause left hemineglect.

Front 71

71. Anosognosia

Back 71

Unawareness of a deficit

Front 72

72. Extinction

Back 72

A tactile or visual stimulus is perceived normally when it is presented to one side only, but when it is presented on the side opposite the lesion simultaneously with an identical stimulus on the normal side, the patient neglects the stimulus on the side opposite the lesion.

Front 73

73. Perseverate

Back 73

Patients w/frontal lobe lesions may have particular difficulty when asked to perform a sequence of actions repeatedly, or to change from one activity to another.

They tend to repeat a single action over an over without moving on to the next one.

Front 74

74. Frontal lobe lesions can cause...

Back 74

1. Personality changes
2. Impaired judgement
3. A cheerful lack of concern over one's illness
4. Inappropriate joking
5. Abulic (opposite of ebullient)
6. Magnetic gait
7. Urinary incontinence

Front 75

75. Prosopagnsia

Achromatopsia

Back 75

Inability to recognize faces

Inability to recognize colors

Front 76

76. Palinopsia

Back 76

Persistence or reappearance of an object viewed earlier

Front 77

77. Blood supply to the brain

Back 77

There are two pairs of arteries that carry all the blood supply to the brain and one pair of draining veins.

The internal carotid arteries form the anterior blood supply, and the vertebral arteries, which join together in a single basilar artery, form the posterior blood supply.

Front 78

78. Circle of Willis

Back 78

The anterior and posterior blood supplies from the carotid and vertebrobasilar systems, respectively, join together in an anastomotic ring at the base of the brain called the circle of Willis.

The main arteries supplying the cerebral hemispheres arise from the circle of Willis.

Front 79

79. What main arteries supply the brainstem and cerebellum?

Back 79

Arise from the vertebral and basilar arteries. These include:

1. Superior cerebellar artery
2. Anterior inferior cerebellar artery
3. Posterior inferior cerebellar artery

Front 80

80. Blood supply to the spinal cord

Back 80

The spinal cord receives its blood from the anterior spinal artery, and from the paired posterior spinal arteries.

The anterior and posterior spinal arteries are supplied in the cervical region mainly by branches arising from the vertebral arteries.

In the thoracic and lumbar regions, the spinal arteries are supplied by radicular arteries arising from the aorta.

Front 81

81. Frontal (anterior) horn of the lateral ventricle

Back 81

Begins anterior to the interventricular foramen of Monro and extends into the frontal lobe

Front 82

82. Body of the lateral ventricle

Back 82

Posterior to the interventricular foramen of Monro, within the frontal and parietal lobes

Front 83

83. Atrium (trigone) of the lateral ventricle

Back 83

Area of convergence of the occipital horn, the temporal horn, and the body of the lateral ventricle.

Front 84

84. Occipital (posterior) horn of the lateral ventricle

Back 84

Extends from the atrium posteriorly into the occipital lobe.

Front 85

85. Temporal (inferior) horn of the lateral ventricle

Back 85

Extends from the atrium inferiorly into the temporal lobe

Front 86

86. Location of the third ventricle

Back 86

Within the thalamus and hypothalamus

Front 87

87. Location of the fourth ventricle

Back 87

Within the pons, medulla, and cerebellum.

Front 88

88. What two foramena in the fourth ventricle permit CSF to leave?

Back 88

1. The lateral foramin of Luschka
2. Midline foramen of Magendie

Front 89

89. What are the cisterns?

Back 89

1. Perimesencephalic cisterns
-Ambient cistern
-Quadrigeminal cistern
-Interpeduncular cistern
2. Prepontine cistern
-contains the basilar artery and the sixt nerves
3. Cisterna magna
4. Lumbar cistern
-contains the cauda equina
-location of spinal tap

Front 90

90. Blood brain barrier

Back 90

Capillary endothelial cells are linked by tight junctions

Front 91

91. What are the circumventricular organs?

Back 91

1. Median eminence
2. Neurohypophysis
3. Area postrema

They interrupt the blood-brain barrier, allowing the brain to respond to changes int eh chemical milieu of the remainder of the body, and to secrete modulatory neuropeptides into the blodostream.

Front 92

92. Area postrema

Back 92

The only paired circumventricular organ, and it is located along the caudal wall of the 4th ventricle in the medulla.

AKA the chemotactic trigger zone; it is involved in detecting circulating toxins that cause vomiting.

Front 93

93. Vasogenic edema

Back 93

Brain tumors, infections, and other disorders can disrupt the blood-brain barrier, resulting in extravasation of fluids into the interstitial space.

This excessive extracellular fluid is called vasogenic edema.

Front 94

94. Cytotoxic edema

Back 94

Cellular damage, for example, in cerebral infarction, can cause excessive intracellular fluid accumulation w/in brain cells, a condition known as cytotoxic edema.

Front 95

95. Vascular headache

Back 95

AKA migraine, as well as the less common but closely related disorder called cluster headache.

Thought to involve inflammatory, autonomic, serotonergic, neuroendocrine, and other influences on blood vessel caliber in the head, leading to headache and other associated symptoms.

Front 96

96. Migraine # 1

Back 96

75% of patients have a positive family history, suggesting a genetic basis.

Symptoms may be provoked by certain foods, stress, eye strain, the menstrual cycle, changes in sleep pattern, and a variety of other triggers.

Often is preceded by an aura, or warning symptoms, classically involving visual blurring, shimmering, scintillating distortions, or fortification scotoma

Front 97

97. Fortification scotoma

Back 97

A characteristic region of visual loss bordered by zigzagging lines resembling the walls of a fort.

Front 98

98. Migraine # 2

Back 98

The headace is often unilateral, but if it is always on the same side, an MRI scan is recommended to rule out a vascular malformation or other lesion.

The pain is often throbbing, and may be exacerbated by light, sound, or sudden head movement.

Duration is typically 30 min to 24 hours, and relief often occurs after sleeping.

Front 99

99. Complicated migraine

Back 99

May be accompanied by a variety of transient focal neurologic deficits, including sensory phenomena, motor deficits, visual loss, brainstem findings in basilar migraine, and impaired eye movements in opthalmoplegic migraine.

Front 100

100. Treatment of migraines

Back 100

Acute attacks usually respond to NSAIDs, anti-emetics, triptans, ergot derivatives, or other medications, and to rest in a dark, quiet room.

Preventative measures include avoiding triggers when possible, and for patients who have frequent attacks, treatment w/prophylactic agents, such as beta-blockers, tricyclic antidepressants, calcium channel blockers, valproate, or methysergide.

Front 101

101. Cluster headache

Back 101

Less than 1/10th as common as migraine; occurs about 5x more often in males than in females.

Typically clusters of headaches occur from once to several times per day every day over a few weeks and then vanish for several months.

Headache pain is extremely sever, often described as a steady boring sensation behind on eye, lasting form about 30-90 min.

It is usually accompanied by unilateral autonomic symptoms, such as tearing, eye redness, Horner's syndrome, unilateral flushing, sweating, and nasal congestion.

Front 102

102. Tension headache

Back 102

AKA tension type headache

A steady dull ache, sometimes described as a bandlike sensation.

Includes the common type of mile to moderate headache that most people experience.

However, some patients have tension-type headaches that occur continuously every day for year. This chronic form of headache is commonly associated w/psychological stress.

Front 103

103. Other causes of headaches

Back 103

1. Acute trauma
2. Intracranial hemorrhage
3. Cerebral infarct
4. Carotid or vertebral artery dissection
5. Venous sinus thrombosis
6. Post-ictal headache
7. Hydrocephalus
8. Psuedotumor cerebri
9. Low CSF pressure
10. Toxic or metabolic derangements
11. Meningitis
12. Epidural abscess
13. Vasculitis
14. Trigeminal or occipital neuralgia
15. Neoplasm

Front 104

104. Psuedotumor cerebri

Back 104

A condition of unknown cause characterized by headache and elevated intracranial pressure with no mass lesion.

Most common in adolescent females, and it is treated w/acetazolamide or, when severe, with shunting procedures.

Front 105

105. Temporal arteritis

Back 105

AKA giant cell arteritis, is an important treatable cause of headache, seen most commonly in elderly individuals.

Vasculitis affects the temporal arteries, as well as other vessels, including those supplying the eye.

The temporal artery is typically enlarged and firm.

Dx made via blood ESR and temporal artery biopsy

Front 106

106. Three mechanisms by which intracranial mass lesions can cause neurologic symptoms

Back 106

1. Compression and destruction of adjacent regions of the brain
2. A mass located w/in the cranial vault can raise the intracranial pressure
3. Mass lesions can displace nervous system structures so severely that they are shifted from one compartment into another, a situation called herniation.

Front 107

107. Mass lesions

Back 107

Can cause both local tissue damage and remote effects thru mechanical distortion of adjacent structures

"Mass effect" is a descriptive term used for any distortion of normal brain geometry due to a mass lesion

Front 108

108. Midline shift

Back 108

Large masses can produce dramatic midline shift of brain structures away from the side of the lesion.

Displacement and stretching of the upper brainstem impairs fucntion of the reticular activating systems, causing impaired consciousness, and ultimately, coma.

The pineal calcification is a useful landmark for measuring the extent of midline shift.

Front 109

109. Cerebral blood flow depends on...?

Back 109

Cerebral perfusion pressure

Defined as the mean arterial pressure - the intracranial pressure

(CPP = MAP - ICP)

Therefore, as the intracranial pressure increases, cerebral perfusion pressure decreases.

Front 110

110. Signs an symptoms of elevated intracranial pressure

Back 110

1. Headache
2. Altered mental status, especially irritability and depressed level of alertness and attention
3. Nausea and vomiting
4. Papilledema
5. Visual loss
6. Diplopia
7. Cushing's triad

Front 111

111. Cushing's triad

Back 111

Hypertension, bradycardia, and irregular respirations

Classic sign of elevated intracranial pressure.

Hypertension may be a reflex mechanism to maintain cerebral perfusion pressure, bradycardia may be a reflex mechanism to the hypertension, and irregular respirations are caused by impaired brainstem function.

Front 112

112. Goal of treating elevated intracranial pressure

Back 112

Reduce it to safe levels, providing time to treat the underlying disorder.

Normal intracranial pressure in adults is less than 20 cm H2O or less than 15 mm Hg.

Another goal of therapy is to keep cerebral perfusion pressure about 50 mm Hg so that cerebral blood flow is maintained.

Front 113

113. How can intracranial pressure be measured?

Back 113

Via lumbar puncture in clinically stable patients.

However, lumbar puncture should not be performed in patients suspected of having severely elevated intracranial pressure due to risk of precipitating herniation.

Via a ventricular drain, intraparenchymal monitor, subarachnoid bolt connected to a pressure transducer in critically ill patients.

Front 114

114. What are the three most important herniation syndromes?

Back 114

1. Transtentorial herniation
2. Central herniation
3. Subfalcine herniation

Front 115

115. Transtentorial herniation

Back 115

Herniation of the medial temporal lobe, especially the uncus (uncal herniation), inferiorly thru the tentorial notch.

Front 116

116. Uncal herniation

Back 116

Heralded by the clinical triad of a "blown" pupil, hemiplegia, and coma.

Compression of CN III, usually ipsilateral to the lesion, produces first a dilated, unresponsive pupil, and later, impairment of eye movements.

Compression of the cerebral peduncles can cause hemiplegia on the contralateral side of the body.

Front 117

117. Kernohan's phenomenon

Back 117

Sometimes in uncal herniations, the midbrain is pushed all the way over until it is compressed by the opposite side of the tentorial notch.

In these cases, the contralateral corticospinal tract is compressed, producing hemiplegia that is ipsilateral to the lesion.

Front 118

118. Central herniation

Back 118

A central downward displacement of the brainstem; can be caused by any lesion associated w/elevated intracranial pressure, including hydrocephalus or diffuse cerebral edema.

Can progress downward through the foramen magnum.

Front 119

119. Tonsilar herniation

Back 119

Herniation of the cerebellar tonsils downward through the foramen magnum.

This condition is associated w/compression of the medulla and usually leads to respiratory arrest, blood pressure instability, and death.

Front 120

120. Subfalcine herniation

Back 120

Unilateral mass lesions can cause the cingulate gyrus and other brain structures to herniate under the falx cerebri from one side of the cranium to the other.

The result is subfalcine herniation.

Front 121

121. Location of epidural hematoma

Back 121

In the tight potential space between the dura and the skull

Front 122

121. Usual cause of an epidural hematoma

Back 122

Rupture of the middle meningeal artery due to fracture of the temporal bone by head trauma.

Front 123

122. Radiological appearance of epidural hematomas

Back 123

Rapidly expanding hemorrhage under arterial pressure peels the dura away from the inner surface of the skull, forming a lens-shaped biconvex hematoma that often does not spread past the cranial sutures where the dura is tightly apposed to the skull.

Front 124

123. Clinical features of epidural hematomas

Back 124

Initially the patient may have no symptoms (lucid interval).

However, within a few hours the hematoma begins to compress brain tissue, often causing elevated intracranial pressure, and, ultimately, herniation and death unless treated surgically.

Front 125

124. Location of subdural hematomas

Back 125

In the potential space between the dura and the loosely adherent arachnoid

Front 126

125. Usual cause of subdural hematomas

Back 126

Rupture of the bridging veins, which are particularly vulnerable to shear injury as they cross from the arachnoid into the dura.

Front 127

126. Clinical features of subdural hematomas

Back 127

Venous blood dissects relatively easily between the dura and the arachnoid, spreading out over a large area and forming a crescent-shaped hematoma.

Two types of subdural hematoma occur:
1. Chronic
2. Acute

Front 128

127. Chronic subdural hematoma

Back 128

Often seen in elderly patients where atrophy allows the brain to move more freely within the cranial vault, thus making the bridging veins more susceptible to shear injury.

This type of hematoma may be seen w/minimal or no known history of trauma.

Oozing slowly, venous blood collects over weeks to months, allowing the brain to accommodate and therefore causing vague symptoms such as headache, cognitive impairment, and unsteady gait.

In addition, focal dysfunction of the underlying cortex may result in focal neurologic deficits.

Front 129

128. Acute subdural hematoma

Back 129

Impact velocity must be high to generate subdural hematoma immediately after an injury.

Associated with high impact, serious injuries.

Prognosis is thus usually worse than w/chronic subdural hematoma or even epidural hematoma.

Front 130

129. Radiological appearance of subdural hematomas

Back 130

Typically are crescent shaped and spread over a large area.

Density depends on the age of the blood; acute blood is hyperdense and therefore bright on a CT.

After 1-2 wks the clot beings to liquefy and may appear isodense.

If there is no further bleeding, after 3-4 wks the hematoma will be completely liquefied and appear uniformly hypodense.

Front 131

130. Mixed density appearance of subdural hematomas

Back 131

If there is continued occasional bleeding, there will be a mixed density appearance resulting from liquefied chronic blood mixed w/clotted hyperdense blood.

Front 132

131. Hematocrit effect in subdural hematomas

Back 132

Sometimes, w/mixed-density hematomas, the denser acute blood settles to the bottom, giving a characteristic hematocrit effect.

Front 133

132. Treatment of subdural hematomas

Back 133

Via surgical evacuation, except for small to moderate sized chronic subdural hematomas, which, depending on the severity of symptoms, can first be followed clinically b/c some will resolve spontaneously.

Front 134

133. Subarachnoid hemorrhage location

Back 134

In the CSF-filled space between the arachnoid and the pia, which contains the major blood vessels of the brain.

Front 135

134. Radiological appearance of subarachnoid hemorrhage

Back 135

Unlike subdural hematomas, blood can be seen on CT to track down into the sulci following the contours of the pia.

Front 136

135. Two types subarachnoid hemorrhage

Back 136

1. Non-traumatic (spontaneous)
2. Traumatic

Front 137

136. Non-traumatic (spontaneous) subarachnoid hemorrhage

Usual cause?

Back 137

Usually presents w/a sudden catastrophic headache, described as "the worst headache of my life".

In most cases, it usually occurs as a result of rupture of an arterial aneurysm in the subarachnoid space.

Less often, it results from bleeding of an arteriovenous malformation and from other causes.

Risk factors for intracranial aneurysm include atherosclerotic disease, congenital anomalies in cerebral blood vessels, polycystic kidney disease, and CT disorders

Front 138

137. Saccular, or berry aneurysms

Back 138

Usually arise from arterial branch points near the circle of Willis.

These are balloon like outpouchings of the vessel wall that typically have a neck connecting it to the parent vessel and a fragile dome that can rupture.

Front 139

138. Where are the most common locations for berry aneurysms?

Back 139

Over 85% occur in the anterior circulation (carotid artery and its branches)

The most common locations are:
1. Anterior communicating artery (30%)
2. Posterior communicating artery (25%)
3. Middle cerebral artery (20%)
4. Vertebrobasilar system (15%)

Front 140

139. Fusiform aneurysm

Back 140

Occasionally the main vessel itself becomes dilated, forming a fusiform aneurysm, which is less prone to rupture than berry aneurysms.

Front 141

140. PComm aneurysm

Back 141

Arising from the internal carotid artery, which can cause a painful third-nerve palsy.

The PComm junction w/the posterior cerebral artery can also give rise to aneurysms, but much less commonly than the PComm junction with the carotid.

Front 142

141. Risk factors for aneurysmal rupture

Back 142

1. Hypertension
2. Smoking
3. EtOH consumption
4. Sudden elevations in BP

Front 143

142. Clinical characteristics of subarachnoid hemorrhages

Back 143

1. Headache
2. Meningeal irritation (causing nuchal rigidity and phototopia)
3. Cranial nerve and other focal neurologic deficits
4. Impaired consciousness, coma, and death

Front 144

143. Prognosis of subarachnoid hemorrhage

Back 144

25% die in the immediate aftermath of the event and thus never reach the hospital

Mortality is about 50%; however, the prognosis is better in mild cases.

In subarachnoid hemorrhage due to ruptured aneurysm, the risk of rebleeding is 4% on the first day and 20% in the first 2 weeks.

Front 145

144. Why is it important to perform a CT scan without contrast?

Back 145

B/c both subarachnoid blood and contrast material appear white on the scan, thus making it difficult to see a small hemorrhage.

CT is better than MRI for detecting acute subarachnoid hemorrhage, although after about 2 days they may no longer be visible on CT.

Front 146

145. Lumbar punctures and subarachnoid hemorrhages

Back 146

Should be performed in suspected subarachnoid hemorrhage w/a negative CT, but not with a positive CT b/c increased transmural pressure across the aneurysm can occasionally precipitate rebleeding.

Front 147

146. Cerebral vasospasm and subarachnoid hemorrhages

Back 147

Following subarachnoid hemorrhage, delayed cerebral vasospasm occurs in about half of all patients, with peak severity about 1 week after the hemorrhage.

This can lead to cerebral ischemia or infarction.

Vasospasm is often treated w/volume expansion and induced hypertension in the ICU.

Such treatment can be done safely after the aneurysm has been clipped.

Front 148

147. Traumatic subarachnoid hemorrhage

Back 148

Caused by bleeding into the CSF from damaged blood vessels associated w/cerebral contusions and other traumatic injuries, is actually more common than spontaneous subarachnoid hemorrhage.

It is usually associated w/severe headache due to meningeal irritation from blood in the CSF.

Deficits are usually related to the presence of other cerebral injuries. Vasospasm is not usually seen.

Front 149

148. Intracerebral or intraparenchymal hemorrhage

Back 149

Location: Within the brain parenchyma in the cerebral hemispheres, brainstem, cerebellum, or spinal cord.

Usual cause: May be traumatic or non-traumatic

Front 150

149. Tramatic intracerebral hemorrhage (contusions)

Back 150

Contusions of the cerebral hemispheres occur in regions where cortical gyri abut the ridges of the bony skull.

Thus, contusions are most common at the temporal and frontal poles.

Front 151

150. Types of contusions

Back 151

Ones that occur on the side of the impact (coup injury) as well as on the side opposite the impact (contrecoup injury) b/c of rebound of the brain against the skull.

Front 152

151. Nontaumatic intracerebral hemorrhage types

Back 152

Include:
1. Hypertensive hemorrhage
2. Lobar hemorrhage

Front 153

152. Hypertensive hemorrhage

Back 153

Most common cause; tends to involve small penetrating blood vessels.

May be related to chronic pathologic effects of hypertension on the small vessels, such as the lenticulostriate arteries, including lipohyalinosis and microaneurysms of Charcot-Bouchard.

Front 154

153. Most common locations for hypertensive hemorrhages

Back 154

1. Basal ganglia (usually the putamen)
2. Thalamus
3. Cerebellum
4. Pons
5. In the ventricles themselves (intraventricular extension/hemorrhage)

Front 155

154. Lobar hemorrhage

Back 155

Bleeding involves the occipital, parietal, temporal, or frontal lobe.

Most common case is probably amyloid angiopathy.

In this condition, deposits of amyloid in the vessel wall of older patients cause vascular fragility.

Unlike hypertensive hemorrhage, the hemorrhages tend to be recurrent or multiple, and they are often more superficial in locations

Front 156

155. Classifications of vascular malformations that can cause intracranial hemorrhage

Back 156

1. Arteriovenous malformations*
2. Cavernous malformations*
3. Capillary telangiectasias
4. Venous angiomas

Only these have a high likelihood of causing intracranial hemorrhage

Front 157

156. Arteriovenous malformations (AVMs)

Back 157

Congenital abnormalities in which there are abnormal direct connections between arteries and veins, often forming a tangle of abnormal blood vessels visible as flow void on MRI scan, but best seen via angiography.

Hemorrhage is usually intracerebral, but it can extend to the intraventricular or subarachnoid space as well.

Treatments include surgical removal, intravascular embolization, and stereotactic radiosurgery.

Front 158

157. Cavernous malformations

Back 158

Abnormally dilated vascular cavities lined by only one layer of vascular endothelium.

Not visible on conventional angiography, but visible via MRI scans.

Have a characteristic MRI appearance, with a central 1-2cm core of increased signal on T1 or T2, surrounding by a dark rim on T2 weighted sequences b/c of the presence of hemosiderin.

Patients present with seizures

Front 159

158. Capillary telangiectasias

Back 159

Small regions of abnormally dilated capillaries that rarely give rise to intracranial hemorrhage.

Venous angiomas are dilated veins visible on MRI scans as a single flow void on MRI and are not known to cause any clinical symptoms themselves, but they can sometimes be seen in association w/cavernous malformations.

Front 160

159. Extracranial hemorrhages

Back 160

Head trauma can also cause hemorrhage in the inner ear, called hemotympanum; hemorrhage in subcutaneous tissues, resulting in Battle's sign; or racoon eyes.

Front 161

160. Subgaleal hemorrhage

Back 161

Scalp hemorrhage can cause profuse bleeding. Hemorrhage in the loose space between the external periosteum and galea aponeurotica can produce a "goose egg" or subgaleal hemorrhage.

Front 162

161. Cephalohematoma

Back 162

In newborns, bleeding during delivery can occur between the skull and external periosteum, called a cephalohematoma, which can occasionally be quite large.

Front 163

162. Hydrocepahalus

Back 163

Caused by excess CSF in the intracranial cavity.

This condition can result from:
1. Excess CSF production
2. Obstruction of flow at any point in the ventricles or subarachnoid space
3. Decrease in reabsorption via the arachnoid granulations.

Front 164

163. Excess CSF production

Back 164

Quite rare as a cause of hydrocephalus; it is seen only in certain tumors, such as choroid plexus papilloma.

Front 165

164. Obstruction of CSF flow

Back 165

Can be produced by obstruction of the ventricular system by tumors, intraparenchymal hemorrhage, other masses, and congenital malformations.

This can occur anywhere along the path of CSF flow, but especially at narrow points such as the foramen of Monro, the cerebral aqueduct, or the fourth ventricle.

Can also occur outside the ventricles in the subarachnoid space as a result of debris or adhesions from prior hemorrhage, infection, or inflammation

Front 166

165. Decreased CSF reabsorption

Back 166

Can cause hydrocephalus when the arachnoid granulations are damaged or clogged.

Decreased reabsorption at the arachnoid granulations is difficult to distinguish clinically from obstruction of CSF flow in the subarachnoid space, an often has similar causes.

Front 167

166. What are the two categories of hydrocephalus?

Back 167

1. Communicating hydrocephalus
-caused by impaired CSF reabsorption in the arachnoid granulations, obstruction of flow in the subarachnoid space, or by excess CSF production

2. Noncommunicating hydrocephalus
-caused by obstruction of flow within the ventricular system.

Front 168

167. Main symptoms and signs of hydrocephalus

Back 168

Similar to those of any other cause of elevated intracranial pressure and can be acute or chronic.

1. Headache
2. Nausea
3. Vomiting
4. Cognitive impairment
5. Decreased level of consciousness
6. Papilledema
7. Decreased vision
8. Sixth-nerve palsies
9. Magnetic gait
10. Incontinence

Front 169

168. Parinaud's syndrome

Back 169

In more severe cases of hydrocephalus, dilation of the suprapineal recess of the posterior third ventricle can push downward onto the collicular plate of the midbrain.

The important abnormality to be aware of is limited vertical gaze, especially in the upward direction.

Front 170

169. Normal pressure hydroephalus

Back 170

A condition sometimes seen in elderly individuals that is characterized by chrnoically dilated ventricles.

Patients typically present w/the clinical triad of gait difficulties, urinary incontinence, and mental decline.

CSF pressure is not usually elevated; problems may result from impaired CSF reabsorption at the arachnoid villi.

Front 171

170. What are the most common brain tumors?

Back 171

1. Glioblastoma
2. Brain metastases
3. Meningioma
4. Astrocytoma
5. Pituitary adenoma
6. Schwannoma
7. Ependymoma

Front 172

171. Gliomas

Back 172

Divided into several types:

Glial tumors arising form astrocytes are called astrocytomas

Classified using the Daumas-Dupont grading system, in which the most malignant is grade IV/IV, or glioblastoma multiforme.

Unfortunately, glioblastoma is relatively common and usually leads to death within 1 year despite maximal resection, radiation, and chemotherapy.

Front 173

172. Meningiomas

Back 173

Arise from the arachnoid villus cells an occur, in order of decreasing frequency, over the lateral convexities, in the falx, and along the basal regions of the cranium.

They grow slowly and appear on CT and MRI scans as homogeneous enhancing areas that arise from the meningeal layers.

In female patients, meningiomas are associated with breast cancer.

Treated by local excision.

Front 174

173. Pituitary adenomas

Back 174

Can cause endocrine disturbances or compress the optic chiasm, usually resulting in a bitermporal visual field defect.

Treatment with dopaminergic agonists often will shrink the tumors.

Front 175

174. Lymphoma of the CNS

Back 175

Has been on this rise in recent years in part due to the increase in HIV.

This neoplasm arises from B lymphocytes and commonly involves regions adjacent to ventricles.

It can often be controlled for several years with chemotherapy and radiation therapy and currently has a median survival rate of close to four years

Front 176

175. Pineal region tumors

Back 176

Relatively uncommon and include pinealomas, germinoma, and rarely teratoma or glioma.

Tumors in this region may obstruct the cerebral aqueduct, causing hydrocephalus, or may compress the dorsal midbrain, causing Parinaud's syndrome.

Front 177

176. What is the most tumor-causing brain hemorrhage?

Back 177

Lung cancer, simply b/c the incidence of lung cancer and metastases to the brain is o high.

Front 178

177. Paraneoplastic syndromes

Back 178

Relatively rare neurologic disorders caused by remote effects of cancer in the body, thought to result from autoimmune mechanisms.

Examples include limbic or brainstem encephalitis, cerebellar Purkinje cell loss, spinal cord anterior horn cell loss, neuropathy, impaired neuromuscular transmission, and opsoclonus myoclonus, which is characterized by irregular jerking movements of the eyes and limbs.

Tumors that most often cause paraneoplastic syndromes include small cell lung carcinoma, breast cancer, and ovarian cancer.

Front 179

178. Infectious meningitis

Back 179

Infection of the CSF in the subarachnoid space. It can be caused by bacteria, viruses, fungi, or parasites.

Except for in elderly, very young, or immunocompromised patients, it is usually heralded by marked signs and symptoms of meningeal irritation, or meningismus.

Front 180

179. Common features of meningeal irritation

Back 180

1. Headache
2. Lethargy
3. Phototopia
4. Phonophobie
5. Fever
6. Nuchal rigidity

Front 181

180. Bacterial meningitis

Back 181

CSF typically has a high WBC count with a PMN predominance, high protein, and low glucose.

Most common pathogens vary on the aptient's age. Treatment, therefore, also depnds on age.

Complications include seizures, cranial neuropathies, cerebral edema, hydrocephalus, herniation, cerebral infarcts, and death

Front 182

181. Brain abscess

Back 182

Another important bacterial infection of the nervous system.

Presents as an expanding intracranial mass lesion, much like a brain tumor, but often with a more rapid course.

Common presenting features include headache, lethargy, fever, nuchal rigidity, nausea, vomiting, seizures, and focal signs determined by the location of the abscess.

Fever is not always present, making the Dx of infection more difficult. The ESR is usually elevated.

Front 183

182. What are the common infecting organisms in brain abscesses?

Back 183

1. Streptococci
2. Baceroides
3. Enterobactericeae
4. S. Aureus
5. Nocardia

Treatment with antibiotics.

*Toxoplasma gondii is also another cause of brain abscess other than bacteria.

Front 184

183. Epidural abscess

Back 184

Can occasionally occur in the spinal canal, and requires prompt diagnosis and treatment.

Common presenting features include back pain, fever elevated peripheral WBC count, headache, and signs of nerve root or spinal cord compression.

Complications include spinal cord compression, paraparesis, and urinary and fecal incontinence.

Treated with surgical drainage and antibiotics.

Common organisms are S. Aureus, streptococci, gram-negative bacilli, and anaerobes.

Front 185

184. Subdural empyema

Back 185

A collection of pus in the subdural space, usually resulting from direct extension from an infection of the nasal sinuses or inner ear.

This condition is treated by urgent surgical drainage and antibiotics.

Front 186

185. Tuberculous meningitis

Back 186

Presents with headache, lethargy, and meningeal signs usually appear over the course of several weeks.

There is often an inflammatory response in the basal cisterns of the brain, which can affect the circle of Willis vessels. If untreated, coma, hydrocephalus, and death ensue.

Front 187

186. Meningeal involvement in tuberculous meningitis results from...?

Back 187

Reactivation of previous tuberculosis infection, and signs of pulmonary tuberculosis are often not present at the time of presentation.

CSF fluid shows an elevated WBC count w/lymphocyte predominance, elevated protein and low glucose.

Front 188

197. What organism is responsible for tuberculous meningitis?

Back 188

Mycobacterium tuberculosis.

Dx can be confirmed by culture, which takes several weeks, or more recently, by PCR.

Treated w/a combo of isoniazid, rifampin, ethambutol, and pyrazinamide.

Front 189

198. Neurosyphilis

Back 189

Caused by the spirochete Treponema pallidum. Transmitted sexually and has various stages that occur at different times after primary infection.

Only in tertiary syphilis do neurologic symptoms present

Front 190

199. Aseptic meningitis in neurosyphilis

Back 190

Meningeal involvement can cause aseptic meningitis, sometimes associated w/cranial nerve palsies, especially involving the optic, facial, and vestibulocochlear nerves.

Later stages can occur following a latency of about 4-15 years. - These are classified as meningovascular syphilis, general paresis, and tabes dorsalis.

Front 191

200. Meningovascular syphilis

Back 191

Chronic meningeal involvement causes an arteritis, typically involving medium-sized vessels, that results in diffuse white matter infarcts.

If untreated, this leads to general paresis.

Front 192

201. General paresis

Back 192

The accumulation of lesions causes dementia, behavioral changes, delusions of grandeur, psychosis, and diffuse upper motor neuron-type weakness.

Front 193

202. Tabes dorsalis

Back 193

Another variant that often coexists w/general paresis. Patients have involvement of the spinal cord dorsal roots, especially in the lumbosacral region, resulting in degeneration of the dorsal columns.

Therefore, these patients have sensory loss in the lower extremities, sensory ataxia with a characteristic high stepping tabetic gait, and incontinence.

Other associated features include Argyll Robertson pupils and optic atrophy.

Front 194

203. Dx of neurosyphilis

Back 194

Based on blood tests for treponemes, together with CSF showing lymphocyte-predominant meningitis.

Treated w/IV penicillin G, and serial lumbar punctures should be performed to monitor the response to therapy.

Front 195

204. Lyme disease

Back 195

Caused by the spirochete Borrelia burgdorferi, carried by Ixodes species of deer tick, which are endemic to certain areas of the US, Europe, and Australia.

Primary infection is often heralded by a characteristic raised rash, which gradually shifts its location and enlarges over days to weeks.

In some cases, neurologic manifestations occur; these usually appear after a delay of several weeks and include a lymphocyte predominant meningitis or mild meningoencephalitis, characterized by meningeal signs and emotional change, with impaired memory and concentration

Front 196

205. Dx & treatment of Lyme disease

Back 196

Via typical clinical features, lumbar puncture, and serological testing.

Untreated cases can eventually show white matter abnormalities on MRI scan.

Lyme disease w/neurologic involvement is treated w/IV ceftriaxone

Front 197

206. Viral meningitis

Back 197

Tends to be less fulminant than bacterial meningitis, and recovery usually occurs spontaneously within 1-2 weeks.

Patient presents w/headache, fever, lethargy, nuchal rigidity, and other signs of meningeal irritation.

Common causes include enteroviruses, such as echovirus, coxsackievirus, and mumps virus. There is no specific treatment for most viral infections of the nervous system.

Front 198

207. Dx of viral meningitis

Back 198

CSF shows an elevated WBC count w/a lymphocytic predominance, normal or mildly elevated protein, and normal glucose.

In the early stages, a PMN predominance may be present.

Front 199

208. Viral encephalitis

Back 199

Viral infections that involve the brain parenchyma.

Unlike typical cases of viral meningitis, the clinical manifestations of viral encephalitis are often quite severe.

The meninges are often also involved, resulting in meningoencephalitis.

Front 200

209. What is the most common cause of viral encephalitis?

Back 200

Herpes simplex type 1 (Type 2 also sometimes causes encephalitis).

The HSV has a tropism for limbic cortex. Patients often present w/bizarre psychotic behavior, confusion, lethargy, headache, fever, meningeal signs, and seizures.

Focal signs such as anosmia, hemiparesis, memory loss, and aphasia may be present as well.

Front 201

210. Other characteristics of herpes simplex encephalitis

Back 201

Also causes necrosis of unilateral or bilateral temporal and frontal structures often visible on MRI scan. Changes in EEG over one or both temporal lobes, CSF shows a mixed lymphocytic-PMN predominance, with elevated protein and normal glucose.

Untreated, it usually progresses w/in days to coma and death.

Therefore, it is essential to initiate therapy promptly w/acyclovir.

Front 202

211. Treatment of other causes of viral encephalitis

Back 202

There are a variety of other causes of viral encephalitis, but unfortunately none of these have a specific treatment. Prognosis depends on the causative agent.

In addition, postinfectious encephalitis can occur, usually several days after a viral infection, with diffuse autoimmune demyelination of the CNS.

Front 203

212. HIV associated disorders of the nervous sytem

Back 203

1. AIDS dementia complex
2. HSV
3. Varicella-zoster virus
4. CMV
5. Progressive leukoencephalopathy
6. Cryptococcal meningitis
7. Toxoplasmosis
8. Primary CNS lymphoma

Front 204

213. Cysticercosis

Back 204

Caused by ingestion of the eggs of teh pork tapeworm Taenia solium. The organism migrates thru the bloodstream to the whole body, forming multiple small cysts in the muscles, eyes and CNS.

Seizures are a common result. Other common features are headache, nausea, vomiting, lymphocytic meningitis, and focal deficits, depending on cyst location. The spinal cord can also be involved, and it can lead to hydrocephalus.

Front 205

214. Dx and treatment of cysticercosis

Back 205

Dx by a history in appropriate populations, by typical radiologic appearance, and by antibody tests of the serum and CSF.

Sometimes, eosinophilia, parasites in the stool, and soft tissue calcifications on Xrays may be present as well.

The condition is treated w/albendazole.

Front 206

215. Murcormycosis

Back 206

Important fungal infection which occurs mainly in diabetics in the rhinocerebral form and also involves the orbital apex.

Rhinocerebral murcormycosis causes opthalmoplegia, facial numbness, visual loss, and facial weakness, with a typical violet coloration of the tips of the eyelids.

Most fungal infections can be Dx via biopsy.

Treatment is with amphotericin B; steroids can exacerbate fungal infections and should be avoided if a fungal infection is suspected.

Front 207

216. Prion

Back 207

A novel protein based infection agent that has been identified in certain neurologic disorders.

They're unique in their ability to transmit diseases from one animal to another, despite the fact that they apparently do not contain DNA or RNA.

Pathologically, diffuse degenereation of the brain and spinal cord occurs, with multiple vacuoles resulting in a spongiform appearance.

Most common illness is Creutzfeldt-Jakob disease.

Front 208

217. Creutzfeldt-Jakob disease

Back 208

Typical presenting features are rapidly progressive dementia, an exacerbated startle response, myoclonus, visual distortions, and ataxia.

EEG often shows periodic sharp wave complexes.

Unfortunately, there is no treatment; progressive neurologic deterioration and death usually occur within 6-12 months.

Front 209

218. Traumatic tap

Back 209

RBCs introduced into the CSF via damage to blood vessels by the spinal needle at the time of lumbar puncture.

As a guideline in a traumatic tap, one WBC is introduced into the CSF for every 700 RBCs.

Front 210

219. What are the three major categories of cerebrovascular diseases?

Back 210

1. Hypoxia, ischemia, and infarction
2. Intracranial hemorrhage
3. Hypertensive cerebrovascular disease

Front 211

220. Hypoxia, ischemia, and infarction

Back 211

Brain oxygen deprivation causes either generalized (ischemic or hypoxic encephalopathy) or focal ischemic necrosis (cerebral infarction).

Front 212

221. Hypotenstion, hypoperfusion, and low flow states (global cerebral ischemia)

Back 212

Generalized hypoxia occurs w/reduced blood O2 content or with reduction of cerebral perfusion pressure, as with hypotension.

Watershep or border zone infarcts occur w/reduced perfusion in those regions of the brain and spinal cord that lie at the most distal edges of arterial supply; the territory between the anterior and middle cerebral artery is most at risk

Front 213

222. Morphology of global cerebral ischemia

Back 213

In the first 12-24 hours after injury, neurons show ischemic cell injury (red neurons).

The most susceptible regions are the pyramidal neurons of Sommer sector of the hippocampus (CA1), the Purkinje cell layer of the cerebellar cortex, and the pyramidal neurons int eh neocortex (pseudolaminar necrosis).

Healing is characterized by gliosis.

Front 214

223. Cerebral infarction from obstruction of local blood supply (focal cerebral ischemia)

Back 214

Can occur either from thrombotic or, more frequently, embolic arterial occlusion.

These events manifest as a stroke - the sudden onset of a neurologic deficit with clinical manifestations referable to the anatomic location of the lesion.

The deficit evolves over time, and the outcome is either permanent or can slowly improve over a period of months.

Venous infarcts are often hemorrhagic; they occur after the thrombotic occlusion of the superior sagittal sinus, an occlusion of the deep cerebral veins.

Front 215

224. Thrombosis in focal cerebral ischemia

Back 215

Usually due to underlying atherosclerosis and most frequently affects the extracerebral carotid system and the basilar artery

Front 216

225. Embolism in focal cerebral ischemia

Back 216

Most commonly involves the intracerebral arteries (most freq the middle cerebral artery distribution).

Emboli can originate from cardiac mural thrombi, valvular disease, and atrial fibrillation.

Fragments can also break off from an arterial mural thrombi most often in the carotid a. or can arise as a paradoxical emboli from the systemic venous circulation that access the cerebral vasculature via atrial or ventricular septal defects.

Front 217

226. Morphology of focal cerebral infarcts

Back 217

Nonhemorrhagic infarcts (bland or anemic infarcts) are evident at 48 hours as pale, soft regions of edematous brain.

The tissue then liquefies, and a fluid filled cavity containing macrophages is lined by reactive glia.

Hemorrhagic infarcts, characteristic of embolic occlusion with reperfusion injury, exhibit blood extravasation,

Front 218

227. Intracerebral hemorrhage

Back 218

Leading cause of death in stroke patients; hypertension is a predisposing factor in 80% of cases.

Front 219

228. Hypertensive intracerebral hemorrhage

Back 219

Most commonly observed in the putamen, thalamus, pontine tegmentum, and cerebellar hemispheres.

Vascular rupture is believed to be due to arteriolar injury with formation of microaneurysms (Charcot-Bouchard aneurysms).

Front 220

229. Morphology of intracerebral hemorrhage

Back 220

Macroscopically, acute hemorrhages exhibit extravasated blood w/compression of the adjacent parenchyma.

Microscopically, resolution shows an area of cavitary destruction of brain w/a rim of gliotic tissue containing pigment-laden macrophages.

Front 221

230. Rupture of subarachnoid hemorrhages/aneurysms occur most often when...?

Back 221

With acute increases in intracranial pressure, such as with straining at a stool or sexual orgasm.

Front 222

231. Morphology of subarachnoid aneurysm

Back 222

At the neck of the aneurysm, the muscular wall and intimal elastic lamina are usually absent or fragmentary, and the wall of the sac is made up of thickened hyalinized intima.

With acutely ruptured aneurysms, blood diffusely fills the subarachnoid spaces.

Front 223

232. Arteriovenous malformations

Back 223

Tangles of numerous, abnormally tortuous and misshapen vessels, containing arteries and veins without an intervening capillary bed, most often in middle cerebral artery territory.

Men are affected 2x as frequently as women; the lesion is most often recognized clinically between ages 10 and 30, presenting as a seizure disorder, intracerebral hemorrhage, or subarachnoid hemorrhage.

Front 224

233. Cavernous hemangiomas

Back 224

Greatly distended, loosely organized vascular channels with thin, collagenized walls; they occur most often in the cerebellum, pons and subcortical regions.

Front 225

234. Capillary telangiectasias

Back 225

Microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma; they occur most frequently in the pons.

Front 226

235. Lacunar infarcts

Back 226

These small, (<15mm), often multiple cystic infarcts result from arteriolar occlusion.

These are most frequently seen in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons.

Clinically, they can be silent or cause serious impairment. B/c of the common involvement of basal ganglia, thalamus, and adjacent white matter, a number of stereotypic syndromes have been described.

Front 227

236. Hypertensive encephalopathy

Back 227

This syndrome is characterized by diffuse cerebral dysfunction (headaches, confusion, vomiting, and convulsion, sometimes leading to coma), with increased intracranial pressure in a hypertensive patient.

Rapid therapeutic intervention is required b/c the syndrome often does not remit on its own.

Postmortem examination may show an edematous brain w/petechiae and necrosis of arterioles.

Front 228

238. Somatic portion of the sensory system

Back 228

Transmits sensory info from the receptors of the entire body surface and form some deep structures.

This info enters the CNS thru peripheral nerves and is conducted immediately to multiple sensory areas in:
1) spinal cord
2) reticular substance of the medulla, pons and mesencephalon
3) cerebellum
4) thalamus
5) areas of the cerebral cortex

Front 229

239. Motor functions of the nervous system

Back 229

1. Contraction of appropriate skeletal muscles throughout the body
2. Contraction of smooth muscle in the internal organs
3. Secretion of active chemical substances by exocrine and endocrine glands.

Front 230

240. Effectors

Back 230

The muscles and glands are called effectors b/c they are the actual anatomical structures that perform the functions dictated by the nerve signals.

Front 231

241. Areas that can control skeletal muscles

Back 231

1. spinal cord
2. reticular substance of the medulla, pons and mesencephalon
3. basal ganglia
4. cerebellum
5. motor cortex

The lower regions control automatic muscle responses to sensory stimuli while the higher regions control deliberate muscle movements controlled by thought processes of the brain.

Front 232

242. Most important function of the nervous system

Back 232

Process incoming information in such a way that appropriate mental and motor responses will occur.

To do this, the the nervous system needs to channel and process information via its "integrative function"

Front 233

243. What determines the directions in which nervous signals travel?

Back 233

The synapses perform a selective action, often blocking weak signals while allowing strong signals to pass, but at other times selecting and amplifying certain weak signals and often channeling these signals in many directions.

Front 234

244. Where does most of the storage of information occur?

Back 234

Most storage occurs in the cerebral cortex.

The basal regions of the brain and spinal cord can store small amounts of information as well

Front 235

245. Facilitation

Back 235

Each time certain types of sensory signals pass through sequences of synapses, these synapses become more capable of transmitting the same type of signal the next time.

Front 236

246. Three major levels of the nervous system

Back 236

1. The spinal cord

2. The lower brain / subcortical level

3. The higher brain / cortical level

Front 237

247. Spinal cord level

Back 237

Neuronal circuits in the cord can cause:
1. walking movements
2. pain reflexes
3. reflexes that stiffen the legs against gravity
4. reflexes that control local blood vessels, GI movements, or urinary excretion

Front 238

248. Lower brain / subcortical level

Back 238

Controls the subconscious activities of the body in the medulla, pons, mesencephalon, hypthalamus, thalamus, cerebellum, and basal ganglia.

Initiates wakefulness, or arousal

Front 239

249. Higher brain / cortical level

Back 239

Stores memories, essential for thought processes, but cannot function by itself.

Front 240

250. Synaptic functions of neurons

Back 240

Impulses may be:

1) blocked in its transmission from one neuron to the next
2) changed from a single impulse into repetitive impulses
3) integrated with impulses from other neurons to cause highly intricate patterns of impulses in successive neurons.

Front 241

251. Two major types of synapses

Back 241

1. Chemical synapses
-almost all synapses used for signal transmission in the CNS are chemical
-utilize neurotransmitters

2. Electrical synapses
-direct open fluid channels that conduct electricity from one cell to the next via gap junctions
-used in smooth muscle and cardiac muscle

Front 242

252. Important property of chemical synapses

Back 242

They transmit signals in a "one-way" direction; that is, from the presynaptic neuron to the postsynaptic neuron.

It allows signals to be directed toward specific goals.

Front 243

253. Differences in neurons

Back 243

1. size of the cell body
2. length, size, and number of dendrites
3. length and size of the axon
4. number of presynaptic terminals

Front 244

254. Two important structure in the terminal boutons

Back 244

1. Transmitter vesicles
-contain transmitter substance that excites or inhibits the postsynaptic neuron

2. Mitochondria
-provide ATP which in turn supplies the energy for synthesizing new transmitter substance.

Front 245

255. Two important components of receptor proteins

Back 245

1. A binding component that protrudes outward from the membrane into the synaptic cleft where it binds the neurotransmitter

2. An ionophore component that passes all the way thru the postsynaptic membrane to the interior of the post synaptic neuron.

Front 246

256. Two types of ionophores

Back 246

1. Ion channel
2. Second messenger activator that is not an ion channel but instead is a molecule that protrudes into the cell cytoplasm and activates one or more substances inside the postsynaptic neuron.

Front 247

257. Cation channels

Back 247

Usually allow sodium ions to pass when opened, but sometimes potassium and or calcium ions as well.

Lined with negative charges which attract the positively charged ions and repel chloride ions and other anions.

Front 248

258. Anion channels

Back 248

Allow mainly chloride ions to pass when the channels open wide enough.

Sodium, potassium, and calcium cations are blocked, mainly b/c their hydrated ions are too large to pass.

Front 249

259. Excitatory transmitter

Back 249

One that opens cation channels

Depolarizes

Front 250

260. Inhibitory transmitter

Back 250

One that opens anion channels.

Hyperpolarizes

Front 251

261. G-proteins

Back 251

Most common type of second messenger proteins. Consists of three parts:
1. an alpha component that is the activator portion of the G-protein
2. a beta component*
3. a gamma component*

*both attached to the alpha component and also to the inside of the cell membrane adjacent to the receptor protein.

On activation by a nerve impulse, the alpha portion separates from the beta and gamma portions and then is free to move w/in the cytoplasm of the cell.

Front 252

262. Functions of the separated alpha components of the G-protein

Back 252

1. Opening specific ion channels thru the postsynaptic cell membrane
2. Activation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) in the neuronal cell.
3. Activation of one or more intracellular enzymes
4. Activation of gene transcription

Front 253

263. Things that cause excitation

Back 253

1. Opening of sodium channels to allow large #'s of positive electrical charges to flow to the interior of the postsynaptic cell.
2. Depressed conduction through chloride or potassium channels, or both.
3. Various changes in the internal metabolism of the postsynaptic neuron.

Front 254

264. Things that cause inhibition

Back 254

1. Opening of chloride ion channels through the postsynaptic neuronal membrane
2. Increase in conductance of potassium ions out of the neuron
3. Activation of receptor enzymes that inhibit metabolic functions.

Front 255

265. Difference between small-molecule, rapidly acting transmitters and neuropeptides

Back 255

Small-molecule, rapidly acting transmitters cause acute responses of the nervous system while neuropeptides usually cause more prolonged actions.

Front 256

266. Examples of small-molecule, rapidly acting transmitters

Back 256

1. ACh
2. Norepinephrine
3. Epinephrine
4. Dopamine
5. Serotonin
6. Histamine
7. GABA
8. Glycine
9. Glutamate
10. Aspartate
11. NO

Front 257

267. Examples of neuropeptides or growth factors

Back 257

1. Hypothalamic releasing hormones

2. Pituitary peptides
-Vasopressin
-Oxytocin
-Prolactine
-Luteinizing hormone

3. Peptides that act on the gut
-Gastrin
-Insulin
-Glucagon

Front 258

268. Areas that secrete acetylcholine

Back 258

1. Terminals of the large pyramidal cells from the motor cortex
2. Several different types of neurons in the basal ganglia
3. Motor neurons that innervate the skeletal muscles
4. Preganglionic neurons of the autonomic nervous system
5. Postganglionic neurons of the parasympathetic nervous system
6. Some postganglionic neurons of the sympathetic nervous system.

Front 259

269. Where is norepinephrine secreted?

Back 259

The terminals of many neurons whose cell bodies are located in the brain stem and hypothalamus.

Specifically, norepinephrine secreting neurons in the locus ceruleus in the pons send nerve fibers to the widespread areas of the brain to control wakefulness and mood.

Also secreted by most postganglionic neurons of the sympathetic nervous system, where it excites some organs but inhibits others

Front 260

270. Where is dopamine secreted?

Back 260

Secreted by neurons that originate in the substantia nigra. The termination of these neurons is mainly in the striatal region of the basal ganglia.

The effect of dopamine is usually inhibition

Front 261

271. Where is glycine secreted?

Back 261

Secreted mainly at synapses in the spinal cord.

It is believed to always act as an inhibitory transmitter

Front 262

272. Where is GABA secreted?

Back 262

Secreted by nerve terminals in the spinal cord, cerebellum, basal ganglia, and many areas of the cortex.

It is believe to always cause inhibition.

Front 263

273. Where is glutamate secreted?

Back 263

Secreted by the presynaptic terminals in may of the sensory pathways entering the CNS, as well as many areas of the cerebral cortex.

It probably always causes excitation

Front 264

274. Where is serotonin secreted?

Back 264

Secreted by the nuclei that originate in the median raphe of the brain stem and project to many brain and spinal areas, especially to the dorsal horns of the spinal cord and to the hypothalamus.

Acts as an inhibitor of pain pathways in the cord, and an inhibitor of the higher regions of the nervous system.

Front 265

275. Where is nitric oxide secreted?

Back 265

NO is especially secreted by nerve terminals in areas of the brain responsible for long-term behavior and for memory.

It is synthesized almost instantly as needed, and it then diffuses out the presynaptic terminals over a period of seconds.

Does not greatly alter the membrane potential but instead changes intracellular metabolic functions that modify neuronal excitability for second, minutes, or longer.

Front 266

276. Synthesis of neuropeptides

Back 266

Not synthesized in the cytosol of the presynaptic terminals, instead they are made as integral parts of large protein molecules by ribosomes in the neuronal cell body.

Goes thru the ER, Golgi apparatus, packaged into vesicle, transported to the tips of axons via axonal streaming.

Process takes a while and hence the reason for a smaller amount of substance released compared to small-molecule transmitters.

Front 267

277. Resting membrane potential of the neuronal soma

Back 267

-65 mV

Front 268

278. At resting potential, where are the sodium ions?

Back 268

Sodium ion concentration is high in the extracellular fluid, but low inside the neuron

Front 269

279. At resting potential, where are the potassium ions?

Back 269

Potassium ion concentration is high inside the neuronal soma but low in the extracellular fluid

Front 270

280. At resting potential, where are the chloride ions?

Back 270

Chloride ion concentration is high in the extracellular fluid but low inside the neuron

Front 271

281. If chloride ions are can easily pass through the permeable neuronal membrane, why does the concentration stay low inside the cell?

Back 271

The -65 mV resting potential repels the negatively charge anions.

Front 272

282. Nernst potential

Back 272

A potential that exactly opposes movement of an ion; potential will be negative (-) for positive ions and positive (+) for negative ions.

Reported in mV and abbreviated as EMF

Front 273

283. Nernst potential equation

Back 273

EMF = ± 61 * log ([inside]/[outside])

Front 274

284. Uniform distribution of electrical potential inside the soma

Back 274

Any change in potential in any part of the intrasomal fluid causes an almost exactly equal change in potential at all other points inside the soma.

This is important b/c it plays a major role in summation of signals

Front 275

285. EPSPs and IPSPs are types of...?

Back 275

postsynaptic excitatory and inhibitory events

Front 276

286. Presynaptic inhibition

Back 276

Caused by release of an inhibitory substance on the outsides of the presynaptic nerve fibrils before their own endings terminate on the postsynaptic neuron.

In most cases, the inhibitory transmitter is GABA which has a specific effect of opening anion channels.

This type of inhibition occurs in many of the sensory pathways in the nervous system.

Front 277

287. Spatial summation

Back 277

The effect of summing simultaneous postsynaptic potentials by activating multiple terminals on widely spaced areas of the neuronal membrane.

Front 278

288. Temporal summation

Back 278

Successive discharges from a single presynaptic terminal, if they occur rapidly enough, can add to one another.

Front 279

289. Facilitation of neurons

Back 279

Often the summated postsynaptic potential is excitatory but has not risen high enough to reach the threshold for firing by the postsynaptic neuron.

When this happens, the neuron is said to be facilitated; it will reach threshold more easily.

Front 280

290. Importance of dendrites in spatial summation

Back 280

The dendrites receive a large spatial area around the motor neuron.

Also, between 80-95% of all the presynaptic terminals of the anterior motor neuron terminate on dendrites compared to only 5 to 20% terminating on the neuronal soma.

Front 281

291. Can dendrites transmit action potentials?

Back 281

Most fail to transmit action potentials b/c their membranes have few voltage-gated sodium channels. However, they do transmit electronic current down the dendrites to the soma.

Front 282

292. What is the drawback of dendritic transmission of electric current?

Back 282

Dendrites are long, and their membranes are thin and at least partially permeable to K+ and Cl- making them "leaky" to electric current.

This is called decremental conduction.

The farther the EPSP is from the soma of the neuron the great will be the decrement and the less will be the excitatory signal that reaches the soma.

Front 283

293. Can dendrite summate EPSPs and IPSPs?

Back 283

Yes, they can in the same way that the soma can.

Front 284

294. Fatigue of synaptic transmission

Back 284

When EPSPs are repetitively stimulated at a rapid rate, the # of discharges by the postsynaptic neuron is at first very great, but the firing rate becomes progressively less in succeeding milliseconds or seconds.

Is important b/c areas of the nervous system can become overexcited; i.e. seizures.

Front 285

295. Mechanism of fatigue in synaptic transmission

Back 285

Mainly exhaustion or partial exhaustion of the stores of transmitter substance int he presynaptic terminals.

Also results from:
1. progressive inactivation of many of the postsynaptic membrane receptors
2. slow development of abnormal concentrations of ions inside the postsynaptic cell.

Front 286

296. Effect of alkalosis on neuronal excitability

Back 286

Normally, alkalosis greatly increases neuronal excitabilty.

Thus, when one hyperventilates, the overbreathing blows of CO2 and therefore elevates the pH of the blood and increases neuronal excitability.

Front 287

297. Effect of acidosis on neuronal excitability

Back 287

Acidosis greatly depresses neuronal activity.

In very sever diabetic or uremic acidosis, coma virtually always develops.

Front 288

298. Strychnine

Back 288

Best known agent that increases the excitability of neurons.

It inhibits the action of some normally inhibitory transmitter substances.

Results in severe muscle spasms.

Front 289

299. Anesthetics and neuronal excitability

Back 289

They increase the neuronal membrane threshold for excitation and thereby decrease synaptic transmission at many points.

B/c they are lipid soluble, it is also plausible that they may change the physical characteristics of the neuronal membranes.

Front 290

300. Synaptic delay

Back 290

The minimal period of time required for all these events to take place is about 0.5 ms:

1. Discharge of transmitter by presynaptic neuron
2. Diffusion of the transmitter to the postsynaptic membrane
3. Action of the transmitter on the membrane receptor
4. And etc...