Mental Status
- Level of Alertness, Attention, and Cooperation:
- Can use test of working memory and attention (e.g., digit span; w-o-r-l-d/d-l-r-o-w)
- What is being tested? Altered consciousness can stem from:
- Damage to brainstem reticular formation
- Bilateral lesions of the thalami or cerebral hemispheres
- Can be mildly impaired in unilateral cortical or thalamic lesions
- Toxic or metabolic factors may lead to impaired consciousness b/c of their effects on these structures
- Orientation
- Memory
- Tests e.g.’s include asking patient to recall 3 items or a brief story for a delay of 3-5 minutes and can evaluate patient’s memory about own history
- What is being tested?
- Problems with immediate memory more likely related to attention
- Difficulties recalling info after 1-5 minutes may implicate the limbic memory structures in the medial temporal lobes and the medial diencephalon
- Language
- Spontaneous speech – observe fluency, phrase length, and abundance of spontaneous speech; observe for paraphasic errors, neologisms, or grammatical errors
- Comprehension
- Naming
- Repetition
- Reading
- Writing
- Gerstmann’s Syndrome
- Deficits in calculations, right-left confusion, finger agnosia and agraphia
- Deficits in all 4 areas implicate the dominant parietal lobe
- Apraxia:Inability to follow a motor command that is not due to a primary motor deficit or language impairment
- Implicates language areas and adjacent structures of the dominant hemisphere
- Neglect and Constructions
- Extinction on double simultaneous stimulation – patients can detect stimulus affected side when presented alone, but when stimuli are presented simultaneously on both sides, only the stimulus on the unaffected side may be detected
- Anosognosia – unawareness of deficits on the affected side of their body
- What is being tested?
- Hemineglect is most common in lesions of the nondominant parietal lobes
- Can occasionally be seen in right frontal lesions, right thalamic or basal ganglia lesions and rarely in lesions of the right midbrain.
- In left parietal lesions, a much milder neglect can be seen affecting the patient’s right side
- Sequencing Tasks and Frontal Release Signs Evaluating for signs of frontal lobe damage such as:
- Perseveration
- Motor impersistence – a form of distractibility in which patients only briefly sustain a motor action in response to a command such as “raise your arms”
- Auditory go-no-go test
- Frontal release signs – e.g., grasp reflexes
- Changes in personality and judgment
- Logic and Abstraction
- Delusions and Hallucinations
- Can be seen in toxic or metabolic abnormalities and other causes of diffuse brain dysfunction as well as in primary psychiatric disorders
- Abnormal sensory phenomena can also be caused by focal lesions or seizures
- Mood
Cranial Nerves
- Olfaction (CN I)
- Not often tested unless specific pathology such as subfrontal tumor is suspected
- Do not use noxious orders as they may stimulate pain fibers from CN V.
- Opthalmoscopic Exam (CN II)
- Allows direct visualization of damage to retina, optic nerve atrophic changes, papilledema and other important abnormalities
- Vision (CN II) check for:
- Visual acuity
- Color vision (red desaturation is a sign of subtle asymmetry in optic nerve function)
- Visual fields
- Visual extinction
- What is being tested?
- Lesions in front of the optic chiasm (eye, optic nerve_ cause visual deficits in one eye while lesions behind the optic chiasm (optic tract, thalamus, white matter, visual cortex_ cause visual field deficits similar for both eyes
- Pupillary Responses (CN II, III)
see p. 59 for full details
- Extraocular Movements (CN III. IV, VI)
- checked by having patient moving eyes without moving their head
- Test for smooth pursuit by having a patient follow a moving object
- Test convergent movements – does patient demonstrate a dysconjugate gaze (eyes not fixated on same point) – results in diplopia(double vision)
- Saccades – eye movements used to rapidly fixate from one object to another (look at my thumb, look at my finger)
- Optokinetic nystagmus – abnormalities in smooth pursuit eye movements
Motor Exam
Only relevant info is detailed here – for full review see pages 63-70
- Observation
- Observe for sings of involuntary movements and tremors – associated with lesions in ganglia or cerebellum (tremors can also occasionally be seen in peripheral nerve lesions)
- Muscle Tone Testing
Evaluates for resistance or rigidity by asking patient to relax and then passively move each limb- helps to distinguish between upper motor neuron and lower motor neuron lesions
- Signs of lower motor neuron lesions – weakness, atrophy, hyporeflexia (reduced reflexes)
- Signs of upper motor neuron lesions – weakness, hyperreflexia, and increased tone.
- In acute upper motor neuron lesions, there is often flaccid paralysis with decreased tone and reflexes; over time (hours to weeks) increased tone and hyperreflexia usually develop
- Increased tone can also occur in basal ganglia dysfunction
- Slow or awkward finger movements or toe tapping in the absence of weakness can signify an abnormality in the corticospinal pathways, but can also occur in lesions of the basal ganglia or cerebellum
- Reflexes
- Plantar Response – tested by scraping an object across the sole of the foot…
- Normal response is downward contraction of the toes
- Abnormal response – Babinski sign – is characterized by an upgoing big toe and fanning outward of the other toes. Toes that do not move up or down (called “silent”) are also considered abnormal.
- 1Abnormal in all adults, although present in infants up to the age of about 1 year
- 2Where localized? Upper motor neuron lesions anywhere along the corticospinal tract
- Frontal release signs – reflexes normally present in infants but that are pathological in adults (from frontal lobe lesions)
- These include the grasp, snout, root and suck reflexes
Coordination and Gait
Re: disturbances of coordination and gait can be caused by lesions in many other systems other than the cerebellum
- Ataxia – abnormal movements seen in coordination disorders;
- Overshoot is commonly seen and is sometimes referred to as past pointing
- Dysdiadochokinesia – abnormal alternating movements
- Appendicular ataxia – affects movements of extremities and is usually caused by lesions of the cerebellar hemispheres and associated pathways
- Can be tested by having patient complete rapid alternating movements, finger-nose-finger test, or heel-shin test
- Truncal Ataxia affects proximal musculature, especially that are involved in gait stability, and is caused by midline damage to the cerebellar vermis and associated pathways
- Romberg test – ask patient to stand with their feet together with eyes open and then to close their eyes – if they then sway or lose balance suggests impairment in the proprioceptive or vestibular systems
- Can be used to implicate the midline cerebellar region (however, similar deficits can be seen with lesions in other parts of the nervous system such as upper or lower motor neurons or basal ganglia)
- Gait
- Evaluate patient’s tandem gait (walking in a straight line heel to toe); patients with truncal ataxia caused by damage tot he cerebellar vermis or associated pathways will have particular difficulty with this task, since they tend to have a wide-based, unsteady gait and become more unsteady when attempting to keep their feet close together.
- Gait apraxia – rare disorder where person can carry out all movements required for gait normally when lying down – but is unable to walk in standing position; believed to be associated with frontal disorders or normal pressure hydrocephalus
Sensory System
- Primary Sensation, Asymmetry, Sensory Level
- Evaluates pain sensation, temperature sensation, vibration sense, joint position sense and 2-oint discrimination (see p. 71 for full details)
- Cortical Sensation, Including Extinction
Test for:
- Graphesthesia – can patient identify letters and numbers that are written onto their palm or fingertips
- Stereognosis – can patient identify objects by touch
- Tactile extinction on double simultaneous stimulation
- Deficits in these domains can be due to lesions in peripheral nerves, nerve roots, posterior columns or anterolateral sensory systems in spinal cord or brainstem, thalamus, or sensory cortex
Coma Exam
Please refer to pages 73 – 78 for full review
- Conditions that can be mistaken for coma:
- Large lesions involving frontal lobes or their connections can cause a condition resembling coma called akinesia or abulia – in this state patient has profoundly decreased initiative and minimal responsiveness, but the eyes are usually open and there may be occasional normal-appearing movements
- Catatonia
- Locked-in syndrome – consciousness and sensation may be normal, but the patient is unable to move because of a lesion in the brainstem motor pathways or because of peripheral neuromuscular blockade