Neurological Signs Flashcards
Dysdiadochokinesis
Lack of coordination when executing rapid alternating movements
Sign of cerebellar impairment
Nystagmus
Fast uncontrollable eye movements.
May be horizontal, vertical, or rotational. May affect one or both eyes.
Ataxic dysarthria
Difficulty in articulating speech (NOT related to problems with the content of speech, i.e. aphasia)
Scanning speech is an example, where a patient splits up words into syllables, often placing the emphasis in the wrong places.
Romberg Sign
When a patient who was able to maintain an erect, balanced stance while eyes were open loses that ability (I.e. starts to sway) upon closing eyes.
Denotes sensory ataxia, where a patient relies heavily on visual input to know the position of their limbs in space.
Vertigo
Sign of vestibular dysfunction (loss of balance info from the inner ear)
Pseudo ataxia of distal limbs
Sign of corticospinal tract disease
Intention tremor
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Cerebellar mutism syndrome (CMS)
Unique postoperative syndrome typically arising 1 to 2 days after resection of a midline posterior fossa tumor
Consists of diminished speech progressing to mutism, emotional lability, hypotonia, and ataxia.
Ataxia
Hallmark of cerebellar disease
Bradykinesia
slow initiation of voluntary movement, poverty of spontaneous movement
Common sign of Parkinson due to loss of the direct pathway.
Chorea
Brief, jerk-like movements.
Defined as irregular, random, abrupt/rapid, and flowing.
Typical of HD (i.e. huntington’s chorea).
Can be a side effect of levodopa.
Athetosis
Slow, writhing movements of flexion, extension, pronation, supination of fingers and hands
Balism
Form of chorea in which large-amplitude jerking or flinging movement, usually of proximal extremities, predominates.
Called hemiballism if it affects only one side of the body.
Dystonia
Sustained muscle contraction causing twisting postures, generally repetitive.
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Tremor
Rythmic and sinusoidal/oscillatory movements caused by alternate contraction of opposing muscle groups.
Types:
- rest (PD/parkinsonism)
- postural (essential tremor, enhanced physiologic)
- Kinetic (ET, cerebellar)
- All
- Task-specific (writing tremor, dyskinesia)
Tics
Intermittent, repeated, and stereotyped movements or sounds under SOME voluntary control
Characterized by internal phenomenology: patient feels the urge to make it, and suppressing the urge leads to “overflow”, need to release the tic.
FOREWARNED AND SUPPRESSIBLE
May be motor or vocal. If both motor and vocal tics present for at least a year, that is the clinical definition of Tourette’s syndrome.
Ex. excessive blinking, throat clearing
Myoclonus
Shock-like or lightning-like SINGLE contraction or jerk. Couldn’t fake it that fast, other degenerative (CJD).
How do you differentiate PD from ET?
In PD, tremors are usually asymmetric rest tremors with accompanying bradykinesia, cogwheel rigidity, micrographia, and shuffling gait.
Family history is more common in patients with ET. These patients exibit symmetric postural/action tremors with no bradykinesia nor rigidity and “shaky-graphia.”
Micrographia
Small, or progressively smaller, handwritting that is difficult to read.
Caused by reduced amplitude of movements (such as those of writting), especially typical of Parkinson’s
Apraxia
Acquired deficit in learned or skilled movements in the presence of intact strength and sensation.
Most cases result from left hemisphere lesions
“limb-as-tool” error
Alzheimers and other neurodegenerative disease patients will present with apraxia where they try to pantomime using a hammer by using their hand as a hammer.
Neglect
Hemispatial neglect is a deficit in attention to and awareness of one side of space, an object, or one’s own body.
It is defined by the inability of a person to process and perceive stimuli on one side of the body or environment that is not due to a lack of sensation
Can be of hemi-space (usually due to inferior parietal lobe lesion), or hemi-object (superior temporal gyrus) modality.
Most common after injury to left parietal lobe.
Agnosia
Not to know
Prosopagnosia
Inability to recognize faces
Agraphia
Inability to write resulting from cortical lesions
Acalculia
Inability to perform simple mathematical/arithmetic tasks
Optic ataxia
inability to reach for visual targers
Ocular apraxia
Inability to direct gaze
Simultagnosia
Inability to appreciate an entire scene, thus being limited to focus only on indivisual objects
Aphasia
Disorder of language
Amusia
Deficiencies in different areas relating to music
Central agraphia
Inability to spell words (either sight words or novel words)
Peripheral agraphia
Loss in the automaticity of forming letters.
These patients may need up to 1 minute to write each letter.
Central alexia
Loss in the ability to either read sight words (these patients read things “phonetically”, sounding out the phoneme of each letter and disregarding the word’s true pronunciation. This problem would not be that evident with Italian or Spanish) OR reading new words (because they can’t read through the word letter by letter; these patients can only read words that are stored in their “sight word” vocabulary)
Peripheral alexia
Difficulty with the rapid “translation” of a letter’s geometrical features into its concept.
These patients read in a painstakingly slow, letter-by-letter fashion.
Apraxia
Loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability.
Disorder of motor planning usually caused by lesion in the cerebrum, and NOT caused by incoordination, sensory loss, and/or inability to comprehend directions.
Fasciculations
Random twitches of denervated motor units visible under the skin.
Fibrillations
Invisible 1- to 5-ms potentials, detected by EMG (electromyography).
Clonus
Rapid successive reflex contractions and relaxation of agonists and antagonists observed mainly at the knee and ankle joints during reflex testing.
Babinski sign
Extensor plantar response (rather than a flexor response) to plantar cutaneous stimulus.
Altered cutaneous reflex typical of an UMN lesion.
NOTE: This is normal in infants until the UMN tracts have become fully myelinated.
