Download Lesions: Lecture 18 Brown-Sequard Syndrome: Ipsilateral UMN

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Lesions: Lecture 18
Brown-Sequard Syndrome: Ipsilateral UMN weakness, Ipsilateral DCML loss,
Contralateral pain and temperature loss below the lesion.
Transverse lesion: Everything below the level of the lesion.
Posterior Cord Syndrome: Loss of proprioception/ fine touch bilaterally.
Anterior cord syndrome: Loss of strength, pain and temperature bilaterally.
Spinal Ganglion Syndrome: Pain and parasthesia limited to dermatome of injured
segment. Think Shingles.
Dorsal Root Syndrome: Complete sensory loss to affected dermatomes with loss of
reflexes.
Lesions: Lecture 20
UMNL: Weakness, Hyper-reflexia, Hypertonia.
LMNL: Weakness, Atrophy, Fasciculations, Hyporeflexia, Hypotonia.
Trochlear Nerve: Eye stays up and in.
Abducens: Eye stays in.
Trigeminal Nerve: Unilateral lesions cause little deficit in jaw movement.
Facial Nerve: UMNL: Contralateral forehead is spared, lower face is weakened.
LMNL: Contralateral forehead and lower face become weak.
Vagal Nerve: Recurent Laryngeal Nerve often injured during surgery, causes
hoarseness.
Spinal Accessory Nerve: Lesion causes ipsilateral loss of scapular elevation, and
cervical rotation away from the lesion.
Lesions: Lecture 23
Anterior Pre-optic Region: Inability to lower body temperature: Hyperthermia in
warm environment.
Posterior Nuclei: Inability to raise body temperature: Hypothermia in cold
environment.
Lateral Nucleus of Hypothalamus: Lesion leads to aphagia and adypsia (refusal to
eat and drink) and ultimately death.
Ventromedial Nucleus: Lesion leads to hyperphagia and polydipsia (Overeating),
and ultimately obesity.
Supraoptic and Paraventricular Nuclei: Lesion leads to Diabetes, lack of thirst
response resulting in hyponatremia.
Lesions: Lecture 24:
Posterior Thalamus: Lesion causes Thalamic Pain Syndrome. Think contralateral
Allodynia. Can be worsened with emotional distress.
VA/VL Lesion: Motor disturbances due to connections with globus pallidus,
cerebellum.
Dorsomedial, anterior lesions: Disorders in consciousness, personality, decreased
motivation, indifference to pain.
Lesions: Lecture 25:
Amygdala lesions: Placidity. Difficulty learning/remembering appropriate
emotional responses. No recognition of fear in others.
Mammillary Bodies, Dorsomedial Nucleus of Thalamus (Karsakoff’s Psychosis):
Impairment of memory with anterograde amnesia. Confabulation present. Seen in
alcoholics, B1 deficiency.
Hippocampus Lesion: Severe anterograde amnesia, minor retrograde amnesia.
Bilateral temporal lobe damage affecting amygdala, most of hippocampus and
parahippocampal gyrus: Placidity, hypersexuality, curiosity of surrounding sensory
stimuli with attempts to taste objects.
Lesions: Lecture 26:
Midline cerebellar vermis or flocculonodular lobe: Truncal ataxia (unsteady gait)
and eye movement abnormalities.
Lateral or intermediate cerebellar vermis lesions: Ataxia of extremities
(appendicular ataxia)
Spinocerebellar Tract Lesion: Freidrich’s Ataxia. Wide based gait, intention tremor.
Lesions: Lecture 27:
None stated in the power point, but this lecture was on the cerebrum, so whatever.
Lesions: Lecture 28:
Schizophrenics lack normal pattern of sleep spindles.
K complexes increase in people with Restless Leg Syndrome.
K complexes are seen in epileptics before a seizure.
Depressed Pt.’s show an increase in time before first period of REM sleep.
Sleep apnea does not allow pt.’s to reach stage III or IV.
Lesions: Lecture 29
Upper Motor Neuron Lesion: Weakness, Hyper-reflexive, Increased tone
LMNL: Weakness, Atrophy, Fasciculations, Hypotonia, Hypo-reflexive.
Pre-Frontal Cortex: BA’s 9, 10, 11, 12, 32, 46:
Loss of initiative; careless, socially unacceptable behavior. (Phineas Gage)
Pre-Motor Cortex: BA4: Results in paralysis/paresis of contralateral body area.
Pre-Motor Cortex BA6: Apraxia: inability to perform voluntary movement, even if
you’re paralyzed.
Frontal Eye Field: Inferior part of BA8: Transient deviation of eyes to ipsilateral side.
Primary gustatory Cortex BA43: Contralateral ageusia (absence of taste.
Parietal Assoc. Cortex: BA5, 7, 39, 40: Neglect syndrome (Contralateral, but typically
on the left), astereognosis (can’t recognize shapes of objects in hand.
Primary Auditory Cortex BA 41 and 42: Lesion causes difficulty in recognizing
distance and direction of sound, especially when the sound comes from the
contralateral side.
Wernicke’s Area (22); Lesion results in receptive aphasia (language
comprehension), and causes word salad. Left inferior division MCA stroke.
Limbic Temporal Cortex: Bilateral lesion causes inability to recognize faces. Seen in
Alzheimer’s disease.
Primary Visual Cortex BA17: Homonymous Hemianopia: Blindness in ½ of visual
field of one or both eyes. Left lesion causes inability to see lateral left field, and
medial right field.
Visual Association Areas: BA18 &19: Visual Agnosia: Loss of ability to recognize
familiar objects or stimuli.
Broca’s Area: BA 44&45: Have trouble speaking and producing language. Lesion for
this would be on dominant hemisphere (Left for a righty due to left superior
division MCA stroke). Will be seen on pt.’s with right paresis. Also called expressive
aphasia.
Lesion between Wernicke’s and Broca’s areas causes conduction aphasia, which
causes repetition.
Lesions: Lecture 30:
Dorsal Root Lesion: Ipsilateral proprioception, fine touch, pain, and temperature
loss at corresponding dermatome.
Posterior Horn Lesion: Ipsilateral loss of pain and temperature in affected
dermatome. No DCML loss.
Lesion to posterior funiculus: Ipsilateral los of fine touch and proprioception.
“sensory ataxia.” Differentiate from cerebellar ataxia d/t no visual involvement.
Lesion of spinal trigeminal nucleus and tract, spinothalamic tract: Ipsilateral loss of
pain and temperature to the face. Contralateral loss of pain and temperature to
body.
Lesion of medial lemniscus and anterior spinothalamic tract: All sensation but pain
and temperature on the contralateral side are lost.
Lesion of Trigeminothalamic and lateral spinothalamic tract: Loss of pain and
temperature on contralateral face, and body.
Complete subthalamic lesion (includes lesions to VPL and VPM) : All sensory info is
lost to contralateral body, including face.
Cortical Lesions: Paresthesia in corresponding regions of contralateral body.
Lesions: Lecture 31:
Lacunar infarct of internal capsule (lenticulostriates of MCA): Hemiplegia including
face. Dysarthria included. Purely motor, not sensory.
Primary motor cortex lesion: Hemiplegia, including facial weakness. Associated
visual, oculomotor and higher cortical deficits.
Corticospinal tract from medulla to C5: Hemiplegia without face weakness.
MCA superior division infarct: Contralateral face and arm weakness and paralysis.