Neuroscience - Block 3 - Neuro Pathologies - Part 1

davidwurbel7's version from 2016-04-04 04:31


Question Answer
Meningioma of the olfactory groove. Compresses olfactory tract and optic nerve, resulting in ipsilateral anosmia, optic atrophy, and contralateral papilledemaFoster Kennedy Syndrome
A persistent, false belief that one is emitting body odors that are foul, and offensive to others. The behavior of others is easily and often misperceived (i.e. someone sniffs, or opens a window, and the ORS person assumes it’s because of them)Olfactory Reference Syndrome (ORS)
The eyes are showing movements when they are not tracking anything, this is bad and indicates brainstem or cerebellar damagePathologic Nystagmus
Eyes move equally in each directionPendular Nystagmus
Fast movement in one direction followed by slow return movement. Described in terms of the fast phase; if it’s to the left, it’s left beating nystagmusJerk Nystagmus
Almost always comes from damage/problems with outer, middle, inner ear, or CN VIII before reaching the cochlear nucleiUnilateral Hearing Loss
Fixation of the stapesOtosclerosis
An inflammation of the middle ear, often accompanied/preceded by viral infection. Is the most common cause of meningitis. Incidence declines with ageAcute Otitis Media
Swimmer’s earOtitis Externa
Deterioration of the organ of Corti. Occurring with aging, it is the most common form of hearing lossPresbycusis
Increased endolymph fluid pressure which enlarges the cochlear duct. Results in episodes of fluctuating hearing loss (distortions of the basilar membrane), tinnitus, and recurrent vertigo. The vertigo can last from 30 minutes to 24 hours, potentially including nausea and vomiting. Difficult to treat and can result in total loss of hearing over a period of years. Episodes are typically unpredictable.Meniere’s Disease
Paralysis of the stapedius muscle, or damage to CN VII, results in hyperacusis, wherein loud noises are not dampened. The condition is most commonly caused, however, by exposure to loud noises/environments (acute like a single gunshot, chronic like playing drums in a rock band).Hyperacusis
During a Weber's Test, a patient hears it louder in affected ear (i.e. patient comes in complaining of hearing loss in left ear, if conductive like ear drum damage, patient hears tuning fork louder in affected (left) ear)Conductive Hearing Loss
During a Weber's Test, a patient will hear the sound louder in the unaffected earSensorineural Hearing Loss
‘Ringing in the ears’ is the sensation of hearing ringing, buzzing, hissing, chirping, whistling, or other sounds. The noise can be intermittent or continuous, and varies in loudness. Could occur with sensorineural or conductive hearing losses, but can also occur independent of any hearing lossTinnitus
A strong negative emotional response triggered by specific sounds. Often accompanied by a flight response. The sounds can be loud or soft (chewing, sniffing, walking, laughing, swallowing, typing, whistling, etc.).Misophonia
Alexia without agraphia is the result of a lesion hereSplenum of the Corpus Collusum
Stroke-induced, results in involuntary flinging of contralateral limbsBallismus
Damage to the Subthalmaic NucleusBallismus
Most common hyperkinetic disorder originating in the basal ganglia. Results from loss of enkephalinergic neurons in the striatum. Dementia sometimes precedes the development of involuntary motor movements. Choreiform movements are the main symptoms. Degeneration of caudate nucleus and subsequent enlargement of ventriclesHuntington’s Disease
Also known as St. Vitus’s dance, and typically occurs between ages 5-15. Usually follows viral infection, strep or acute rheumatic feverSydenham’s Chorea
Symptoms include ‘Milkmaid’s grasp’, choreic movements, darting tongue, pronator sign, and behavioral or cognitive changes. Typically resolves within 6-10 weeks, although relapses do occurSydenham’s Chorea
Parkinson’s Disease is the most common type of this type of disorderHypokinetic Dyskinesia
Characterized by Bradykinesia - Poverty and slowness of movement. Tremor - Only seen while extremity is at rest; disappears during sleep. Rigidity - Resistance to passive limb movements. Tremor and rigidity is called Cogwheel rigidity. Usually begins between ages 40-70. Primary treatment with L-Dopa. Secondary treatment Pallidotomy, Thalidotomy and Deep Brain StimulationParkinson's Disease
Tremors that are always present regardless of motion or restEssential Tremors
Syndrome of sustained muscle contractions, frequently causing twisting and repetitive movements, or abnormal postures. Thought to occur following lesions of the lentiform nucleusDystonia
Characterized by multiple motor tics and at least one verbal tic. Is mild in most cases, decreases in severity from adolescence to adulthood. Unlike other kinetic disorders, the tics are non-rhythmic and temporarily suppressible, and usually preceded by a premonitory urge. Copralalia (obscenities), echolalia (repeating other’s words), palilia (repeating one’s own words) are rareTourette’s Syndrome
Copper accumulation in the liver (enzyme deficiency) results in chronic fatigue, hepatitis, cirrhosis. Copper is also released by the liver into blood (not bound to ceruloplasmin) and deposits in eyes, kidneys and brain. Neurological symptoms include cognitive impairment, changes in behavior, hypo- or hyper-kinetic symptoms (dystonia, etc.) as copper accumulates mostly in the lentiform nuclei. Can affect any age, other symptoms include cardiac arrythmias, infertility, hypoparathyroidism, hepatic encephalopathWilson’s Disease
Copper deposits in the eyesKayser-Fleischer Rings
A lesion to the Globus pallidusTourettes
A lesion to the Striatum/neostriatumHuntington’s Disease
A lesion to the Subthalamic nucleusBallismus
A lesion to the substantia nigraParkinson’s Disease
A lesion to the various structures due to copper dispositionWilson’s Disease
Neural damage in the infant due to hypoxia during the birthing processCerebral Palsy
This patient is unable to express, can understand but cannot repeatBroca's Aphasia
This patient is unable to express, can understand and can repeatTransmotor Cortico
This patient is able to express, cannot understand and cannot repeatWernicke's Aphasia
This patient is able to express, cannot understand and can repeatTranssensory Cortico
This patient is able to express, can understand but cannot repeatConduction Aphasia
This patient is unable to express, cannot understand and cannot repeatGlobal Aphasia
Unable to perform repetition taskConduction Aphasia
Damage to this area causes conduction aphasiaArcuate Fasciculus
Damage to this causes Akinetic mutism (patients don’t tend to move or speak) or tactile agnosiaAnterior (genu) Corpus Callosum Lesion
Damage to this causes alexia without agraphiaSplenium of the Corpus Callosum Lesion
Loss of ability to comprehend written/spoken language. Patients can still speak, but with decreased or nonexistent semantic or syntactical meaning. They typically can’t understand themselvesWernicke’s Aphasia
Wernicke’s Aphasia is also known asReceptive Aphasia
Inability to transform thoughts into words (loss of speech production). Muscles of the face and mouth are not affected; patients can still eat, for example. This tells us that the speech impairment is not likely due to motor problems/nerve lesionsBroca’s Aphasia
Broca’s Aphasia is also known asExpressive Aphasia
Lesion of the arcuate fasciculus. Speech comprehension is intact, while speech production is variably affected. Patient has great difficulty in repeating words, and in naming tasksConduction Aphasia
Lesion of Wernicke’s and Broca’s areas in the non-dominant hemisphere: Results in loss of comprehension of inflection/emotional content in speechReceptive Dysprosody
Lesion of Wernicke’s and Broca’s areas in the non-dominant hemisphere: Results in loss of use of inflection/emotional content in speechExpressive Dysprosody
Damage near Wernicke’s area. Naming, reading, comprehension are poor, but speech fluent and grammatical. Repetition is good. Patient tends to substitute ‘similar’ words often (like pencil for pen, or apple for orange). Speech is generally better than in Wernicke’s aphasiaTranscortical Sensory Aphasia
Poor comprehension, poor speech production from damage to both Wernicke’s and Broca’s areas. May include conduction aphasia deficits. Most severe aphasiaGlobal Aphasia
Global aphasia is also known asMixed Transcortical Aphasia
The area near Broca’s (watershed) is damaged, but not Broca’s. Patient has great difficulty producing speech, but has no problem repeating (arcuate fasciculus is still intact). Comprehension, reading, naming are goodTranscortical Motor Aphasia
Not recognizing an object visuallyVisual Agnosia
Inability to name or distinguish colorsColor Agnosia
Inability to recognize an object by touch of either left or right handTactile Agnosia
Loss of ability to distinguish between stationary and moving objectsMovement Agnosia
Inability to recognize the presence of disease in one’s selfAnosognosia
Inability to recognize a part of the bodyAutotopagnosia
Inability to recognize spatial positioning of body partsStatognosis
A form of tactile agnosia but in both handsAstereognosis
Inability to recognize speech, animal sounds, mechanical soundsAuditory Agnosia
Inability to recognize facesProsopagnosia
Following a hemispheric lesion, the person is unable to perceive stimuli from the contralateral environment or body. Left side neglect (right side lesion) more common. Person ignores stimuli on the affected side, will likely show constructional apraxia with neglect (see next slide), ignore food on one side of the plateNeglect
Copies the drawing accurately, but only one sideNeglect
Cannot reproduce the drawing, and ignores one half of itConstructional Apraxia with Neglect
Specific for not perceiving one side of the body. It may be caused by Neglect, but also occurs sometimes after paralysis of the limb. Patient is usually indifferent about the ‘missing’ limbAsomatognosia
Subtype of Asomatognosia in which the patient shows ‘delusional’ misidentification, or confabulation, with regards to the affected limbSomatoparaphrenia
Result from damage to parietal or frontal lobe. Angular gyrus (39), Supramarginal gyrus (40) and pre-motor area (6) are likely locationsApraxia
Inability to correctly imitate hand gestures and voluntarily ‘pantomime’ tool use, i.e. pretend to brush one's hair when asked. Dominant parietal lobeIdeomotor Apraxia
Inability to correctly perform a series of movements to accomplish a task (putting on shoes and socks). Items may be used incorrectly (brushing hair with a pen). Dominant parietal lobeIdeational Apraxia
Inability to perform facial or oral motor acts on command (ie. licking lips). Dominant parietal lobe.Facial Apraxia
Inability to draw simple objects. Non dominant parietal lobe.Constructional Apraxia
Inability to dress (button shirt, etc). Often associated with neglect. Non dominant parietal lobe.Dressing Apraxia
Inability to voluntarily open the eyes. (non-dominant parietal or frontal lobe).Lid Opening Apraxia
A rare disorder of oculomotor function due to bilateral lesions of the parietal and occipital lobes. Inability to execute voluntary movements in response to visual stimuli. Individual has normal visual fields and acuity, but will fixate on only one object, and is unable to recognize other visual stimuliBalint’s Syndrome
Inability to move the hand towards an object by visual guidance (kinda like Dysmetria except the damage isn’t cerebellar)Optic Ataxia
Paralysis and/or impairment of visual fixation, or more simply put, inability to voluntarily control one’s gaze. They seem to lack the ‘saccadic’ jump needed to acquire new visual targetsOptic Apraxia
Inability to recognize more than one object at the same time. Look at place setting, can only see fork or spoonSimultagnosia
Disorder of oculomotor function due to bilateral lesions of the parietal and occipital lobes. Inability to execute voluntary movements in response to visual stimuli. Individual has normal visual fields and acuity, but will fixate on only one object, and is unable to recognize other visual stimuli.Balint’s Syndrome
When damaged Contralateral paralysis, hyperreflexia, BabinskiPrimary Motor Cortex
Damage to this region can result in ApraxiasPremotor Cortex
Damage symptoms can vary, but might include Alien Hand SyndromeSupplementary Motor Area
Damage to area 39 (Angular gyrus) and often area 40 as well (supramarginal gyrus). Dominant hemisphere only. Symptoms include Contralateral hemi- or quadrantinopia, Right-left confusion, Finger agnosia, Agraphia, DyscalculiaGerstmann’s Syndrome
Unilateral lesion results in maybe a little hearing loss. But bilateral damage would result in thisCortical Deafness
Ipsilateral anosmia would be the result of damage to thisPrimary Olfactory Cortex
Contralateral upper quandrantinopia would be the result of damage to thisMeyer’s Loop
Degeneration of ACh neurons in the nucleus basalis of Meynert. Neuro-degenerative disorder (irreversible and progressive). Characterized by Loss of ACh neurons in nucleus basalis, Beta-amyloid plaque accumulation and Neurofibrillary tanglesAlzheimer’s Disease
Age related ischemic damage to white matter results in an Alzheimer’s like dementia. Follows hypertension or other vascular problems. Progressive dementia, rigidity and gait problemsBinswanger’s Subcortical Leukoencephalopathy

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