Is there hypo or hyperreflexia in a patient of stroke

Reading File

Finding Sources

Reading File

Here is a thorough, textbook-backed answer:

Reflexes in Stroke: Hypo vs. Hyperreflexia

Stroke is a upper motor neuron (UMN) lesion, and the reflex pattern depends entirely on the phase after onset.

Phase 1 - Acute Phase (hours to a few days): HYPOREFLEXIA / Areflexia

Immediately after a stroke, the affected limbs show flaccid paralysis with reduced or absent deep tendon reflexes. This is called "cerebral shock" (analogous to spinal shock in spinal cord injury). The cortical input to the spinal cord is suddenly interrupted, causing a transient depression of all spinal cord activity below the lesion.

Key features of the acute phase:

Flaccid (floppy) limbs
Hypotonia
Hyporeflexia or areflexia
Babinski sign may already be positive (extensor plantar response)
No clonus

Phase 2 - Subacute/Chronic Phase (days to weeks onward): HYPERREFLEXIA

As the spinal cord recovers from shock, the loss of UMN inhibition becomes the dominant feature. The spinal reflex arcs are now released from cortical control, leading to exaggerated responses.

Key features of the chronic phase:

Hyperreflexia - brisk, exaggerated deep tendon reflexes
Spasticity - velocity-dependent increase in muscle tone
Clonus - rhythmic involuntary contractions (especially at the ankle)
Positive Babinski sign (extensor plantar response)
Clasp-knife rigidity

This is the classic "UMN syndrome", confirmed by multiple authoritative sources:

"The full upper motor neuron syndrome of spasticity and hyperreflexia may be absent in the acute phase... [but develops over time]"

Goldman-Cecil Medicine, p. 2000

"The weakness is of the upper motor neuron type and is usually accompanied by other pyramidal signs such as spasticity, hyperreflexia, and extensor plantar responses."

Harrison's Principles of Internal Medicine 22E, p. 2289

Summary Table

Feature	Acute Stroke	Chronic Stroke
Tone	Flaccid (hypotonia)	Spastic (hypertonia)
Reflexes	Hyporeflexia / absent	Hyperreflexia
Plantar response	Extensor (Babinski +)	Extensor (Babinski +)
Clonus	Absent	Present
Mechanism	Cerebral shock	Loss of UMN inhibition

Why This Matters Clinically

In the acute ER setting, a stroke patient may paradoxically show flaccid weakness with reduced reflexes - this does NOT mean it is a lower motor neuron (LMN) lesion.
The positive Babinski sign is present from the very start in UMN strokes, even during the flaccid phase - this is the key differentiating clue from a true LMN lesion.
Over weeks, spasticity and hyperreflexia become the dominant findings, which can contribute to post-stroke complications like contractures and abnormal gait patterns.

This is a shared conversation. Sign in to Orris to start your own chat.