ADD-ONS / GENERAL NEUROLOGY

Signs and symptoms of cerebral lesions

David Goldemund M.D.
Updated on 08/03/2024, published on 12/09/2023

cerebral lesions manifest through diverse signs and symptoms that reflect the regional specialization of the brain
based on neurologic examination, the probable location and etiology of the lesion can be assumed

Frontal lobe

behavioral symptoms (prefrontal syndrome)
- altered personality
- emotional lability
- disinhibition and socially inappropriate behavior
- abulia or loss of will, particularly when the lesion involves medial frontal regions
motor symptoms
- hemiparesis if motor areas are involved
- altered speech production in lesions affecting Broca’s area in the dominant hemisphere
cognitive symptoms
- executive dysfunction
- memory deficits (particularly working memory)
epileptic seizures

Temporal lobe

large lesions can quickly lead to temporal conus syndrome
Wernicke’s aphasia – impaired comprehension and fluent but nonsensical speech output (superior temporal gyrus in the dominant hemisphere)
auditory agnosia – difficulty in recognizing sounds despite intact hearing
memory impairment
complex focal seizures

Parietal lobe

lesion in the dominant hemisphere leads to impaired symbolic functions (aphasia, anosmia, acalculia, alexia, agraphia, apraxia, etc.)
sensory symptoms
- contralateral hemihypesthesia to various sensory modalities
- astereognosis (difficulty in recognizing objects by touch, astereognosis, lesions affecting the postcentral gyrus)
- agnosia for pain or temperature (may also be caused by thalamic lesion)
visuospatial impairment
- contralateral neglect syndrome (usually caused by lesions in the nondominant hemisphere), often accompanied by hemianopsia
- optic ataxia (posterior parietal cortex)
- Balint syndrome – a triad of optic ataxia, oculomotor apraxia, and simultanagnosia (more commonly seen in bilateral parietal lesions)
- impaired spatial orientation
cognitive and language impairment
- Gerstmann syndrome (includes agraphia, acalculia, finger agnosia, and left-right disorientation; angular gyrus is usually affected)
- anomia (difficulty in naming objects, particularly when the dominant hemisphere is affected)
  - caused by damage to various brain regions rather than a single, well-localized area
  - lesions can be found in the dominant hemisphere and often involve the angular gyrus, the middle and inferior temporal gyri, or regions of the frontal lobe, specifically the dorsolateral prefrontal cortex

Neglect syndrome

neglect syndrome, also known as hemispatial neglect or unilateral neglect, is characterized by a failure to attend to or be aware of stimuli presented on one side of space, typically opposite to the side of the brain injury
typically caused by lesions in the right hemisphere, resulting in neglect of the left side of space
- exact locations differ based on the modality affected
it may affect both motor and sensory modalities (visual, auditory, and tactile neglect)
- visual neglect is the most common, characterized by a lack of awareness of visual stimuli presented in the neglected visual field (a patient may only draw or describe objects on the right side of a scene, ignoring those on the left)
- individuals may neglect motor actions related to the affected side (they may fail to eat food from the left side of a plate or neglect to groom the left side of their body)
anosognosia = a lack of awareness or insight into one’s neurological disorder (e.g., patient neglects hemiparesis)
neglect syndrome can significantly impact daily functioning and rehabilitation efforts(specific techniques are required)

Gerstmann syndrome

a constellation of symptoms resulting from damage (usually stroke) to the dominant (usually left) parietal lobe, specifically the angular gyrus
the key features of Gerstmann syndrome include:
- agraphia/dysgraphia – difficulty with writing, ranging from a complete inability to write (agraphia) to various errors in written expression (dysgraphia)
- acalculia – impaired ability to perform basic arithmetic operations
- finger agnosia – difficulty in distinguishing and recognizing the fingers of one’s own hands
- left-right disorientation – Confusion or inability to correctly identify the left and right sides of one’s body in the external environment
Gerstmann syndrome is distinct from more generalized cognitive deficits seen in parietal lobe strokes, as it specifically involves the aforementioned cluster of symptoms

Occipital lobe

homonymous hemianopia
cortical blindness (complete loss of vision with preservation of pupillary light reflex and intact ocular structures)
visual agnosia – inability to recognize visually presented objects despite intact vision
Anton-Babinski Syndrome – a rare neurological condition characterized by cortical blindness with the paradoxical denial of visual loss (agnosia)
Reverse Anton Syndrome – patients claim to be blind but actually have preserved vision
achromatopsia – inability to perceive color
- usually caused by stroke lesions in the medial occipital lobe, typically involving the lingual and fusiform gyri
palinopsia – abnormal persistence or recurrence of visual images
- derived from the Greek word “palin” for “again” and “opsia” for “seeing
- images are long lasting or intens
Balint syndrome (usually involves parieto-occipital lesion)

Anton syndrome

a rare condition named after the Austrian psychiatrist Gabriel Anton, in which individuals with cortical blindness, typically resulting from bioccipital lesions, deny their blindness
despite being unable to see, patients with Anton’s syndrome may adamantly insist that they can see normally
this phenomenon is often accompanied by confabulation, where patients fabricate explanations or scenarios to explain their visual experiences despite lacking true visual perception
patients may resist efforts to provide appropriate care or rehabilitation
this syndrome is proof of the complex interplay between perception, awareness, and higher cognitive functions

Balint syndrome

a rare disorder characterized by a triad of symptoms involving visuospatial dysfunction, first described by the Hungarian neurologist Rezső Bálint in 1909
typically associated with bilateral lesions in the parietal and occipital lobes, particularly in the posterior parietal cortex and the superior occipital gyrus
symptoms of Balint syndrome:
- simultanagnosia
  - difficulty perceiving the visual field as a whole
  - patients may only be able to focus on one object at a time and struggle to perceive multiple objects simultaneously; this results in a fragmented perception of their surroundings
- optic ataxia
  - patients with optic ataxia have difficulty accurately reaching for objects in their visual field, even though their vision and motor function are otherwise intact
  - they may misreach or fumble when attempting to interact with objects
- ocular apraxia
  - patients have difficulty voluntarily directing their gaze toward specific objects or locations despite having intact visual acuity
  - they may exhibit difficulty shifting their gaze between objects or initiating saccadic eye movements
hemineglect, which usually results from lesions in the temporoparietal junction, should be distinguished from Balint syndrome

Basal ganglia

hemiparesis or hemiplegia with hemisensory deficit (due to a lesion of the internal capsule)
dysarthria
impaired level of consciousness (sign of rostral brainstem involvement)
hyperkinetic movements (tremor, chorea, balism)
impaired saccadic or smooth pursuit eye movements

Thalamus

contralateral hemihypesthesia and hemiparesis (less prominent unless the internal capsule is involved) → lacunar stroke
hemichorea, hemiataxia, hemibalism (Takahashi, 2012)
oculomotor dysfunction due to cranial portion
- skew deviation (deviation of one eye upward, the other downward); more commonly seen in brainstem lesions
- upward gaze palsy (due to the disruption of the thalamocortical or brainstem-thalamic pathways)
- impaired smooth pursuit movements (the thalamus has connections with the parietal and occipital lobes that are involved in visual tracking)
thalamic neglect syndrome (right) or aphasia (left)
thalamic pain
thalamic hemorrhage usually affects the diencephalon and mesencephalon directly or by compression; even a small-volume thalamic hematoma can lead to aqueduct blockage or transtentorial herniation

Cerebellum

neocerebellar and/or paleocerebellar syndrome (ataxia, dysmetria, dysdiadochokinesia, intention tremor, hypotonia)
dysarthria
nystagmus
nausea, vomiting, and headache due to intracranial hypertension
in larger lesions with brainstem compression, hemiparesis and cranial nerve palsy may occur
altered level of consciousness (LOC) and breathing disorders usually depend on the size of the lesion and the degree of brainstem compression
executive dysfunction

Brainstem

mesencephalic lesions are typically small
- oculomotor paresis, varying degrees of various pathways involvement
pontine lesions are divided according to their localization into basal-tegmental, bilateral tegmental, massive, and small unilateral tegmental [Chung, 1992]
- decreased level of consciousness (most common)
- bulbar and respiratory dysfunction, bradycardia, quadriplegia, cranial nerve palsies
- risk of CSF blockade with the development of acute obstructive hydrocephalus
- extensive pontine hemorrhage has a poor prognosis
primary lesions in the oblongata lead to bulbar symptoms, often hemiparesis, cerebellar ataxia due to pathway involvement, and possibly respiratory dysfunction
hemorrhages in the posterior fossa may be associated with persistent, days-lasting hiccups, which may contribute to the worsening of respiratory insufficiency

→ Brainstem syndromes
→ Brainstem reflexes